PReD-Bench/PRed-Bench huggingface dataset:
Vitamin D receptor gene polymorphism is associated with multiple myeloma
Authors: Meiying Lin
Hongbing Rui
Xiaoqiang Zheng
Ying Liu
Journal: Journal of Cellular Biochemistry (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SNP; gene polymorphism; multiple myeloma; vitamin D receptor.
Affiliations: Department of Hematology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.

Abstract:  Objectives: The aim of this study was to explore the Vitamin D receptor (VDR) gene polymorphism and its association with multiple myeloma (MM) development. Methods: The peripheral blood of 40 MM cases and 84 healthy controls were collected. Polymerase chain reaction (PCR) and DNA sequencing were applied to detect VDR gene polymorphism (including: FokI, BsmI, ApaI, and TaqI). SHESIS biological information software was used to analyze genotypes, alleles, linkage disequilibrium (LD), haplotype distribution, and their association with MM. Results: Compared with controls, the MM group had a significantly higher frequency of the A allele in BsmI site (8.7% vs 2.4%) and C allele in the TaqI site (10.5% vs 3.6%). These two alleles were closely associated with an increased risk of MM (P = .025; P = .030). The highly rare genotypes (BsmI-AA and TaqI-CC) were found in one patient with MM. Conclusion: VDR gene polymorphisms may be a molecular marker of MM risk. 

Retracted: No

PubPeer comments:
  These pixel esteems meddle with other picture preparing and make the drive clamor in the picture which ought to be filtered This paper appears to be computer manipulated - see https: arxiv.org pdf 2107.06751v1.pdf ,
MiR-320c prevents the malignant development of cervical cancer by regulating GABRP level
Authors: C Zhou
Y Huang
W Pan
P-C Jiang
Y Li
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-320c; cervical cancer; therapeutic target; biological behaviors; clinical characteristics
Affiliations: Department of Gynecology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China. .

Abstract:  Objective: This study aims to explore the role of microRNA-320c (miR-320c) in regulating biological behaviors of cervical cancer and the potential mechanism, thus providing experimental references for developing therapeutic target of cervical cancer. Patients and methods: Differential expressions of miR-320c in cervical cancer samples and normal cervical tissues were determined. Potential association between miR-320c level and clinical characteristics of cervical cancer patients was analyzed. After overexpression of miR-320c, migratory potential changes in HeLa, and C33-A cells were examined. At last, target gene binding to miR-320c was predicted online and its involvement in the malignant development of cervical cancer was finally explored. Results: It was found that miR-320c was lowly expressed in cervical cancer tissues. Compared with cervical cancer patients with high expression of miR-320c, those with low expression had higher rates of lymphatic metastasis and distant metastasis. Besides, the overexpression of miR-320c markedly inhibited migratory potential in HeLa and C33-A cells. GABRP was verified to be the target gene binding to miR-320c. Notably, GABRP was able to reverse the role of miR-320c in regulating migratory potential in cervical cancer. Conclusions: MiR-320c is capable of inhibiting migratory potential in cervical cancer by targeting GABRP, which may be utilized as a therapeutic target of cervical cancer. 

Retracted: No

PubPeer comments:
 Fig 3E.  A negative correlation between expression levels of miR-320c and GABRP in cervical cancer tissues . ![file] For comparison:  Here is a small collage of the plots (h t [Elisabeth Bik] ): ![] , 
 Fig 1D.  Overall survival in cervical cancer patients expressing high or low level of miR-320c . ![file] It is another manifestation of  Hoya s Law for J.BUOn ERMPS :  When 40 or 50 cases of any given cancer are dichotomised into half-groups of high- or low-expression of any given noncoding RNA, survival rate for one half-group or both always drops to 0% at 75 months. ,
miR-138 suppresses cell proliferation and invasion by inhibiting SOX9 in hepatocellular carcinoma
Authors: Kai Liu
Songyang Liu
Yingchao Wang
Wei Zhang
Bai Ji
Yahui Liu
Journal: American journal of translational research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hepatocellular carcinoma; SOX9; invasion; miR-138; proliferation.
Affiliations: Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University Changchun 130021, Jilin Province, China.

Abstract:  Accumulating evidence suggests that miR-138 expression was frequently downregulated in different cancer types and involves in the progression of tumorigenesis. However, the biological role and molecular mechanism of miR-138 involvement in hepatocellular carcinoma (HCC) still remains largely unknown. Therefore, in the present study, we investigated the role of miR-138 in the progression of HCC. We found that miR-138 expression levels were significantly downregulated in HCC tissues and cell lines compared with the corresponding noncancerous liver tissues and normal hepatic cell line. In addition, we also found that enforced expression of miR-138 inhibited proliferation, colony formation, migration and invasion in HCC cells. Using a luciferase reporter assay, SOX9 was confirmed as a direct target of miR-138. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay showed that overexpression of miR-138 in HCC cells significantly inhibited SOX9 expression on mRNA level and protein level. Furthermore, SOX9 expression was significantly upregulated in HCC tissues and cell lines, and its mRNA expression is negative correlated with miR-138 expression in clinical HCC tissues (r=-0.689, P&lt;0.01). Of note, downregulation of SOX9 performed similar effects with overexpression of miR-138. These findings suggested that miR-138 functioned as a tumor suppressor in HCC partially via repressing SOX9 expression. 

Retracted: Yes

PubPeer comments:
 Fig 5B.  SOX9 expression on ... protein level were detected HCC tissues and adjacent no-cancerous tissues. GAPDH was used as a control. ![file] The right-hand three lanes of the loading control seem to overlap with the band labeled  1 e.g. in the context of [Zhang et al (2015)] . ![] , 
 Retracted [15 November 2021] .  Falsified materials and or data reported in this publication were detected by a knowledgeable reader and subsequently confirmed by further investigation of editorial office. Therefore, the entire article has been retracted in accordance with this journalu2019s policy and editorial decision. ,
Polymeric nanospheres modified with YIGSR peptide for tumor targeting
Authors: Praveen K Dubey
Deepak Singodia
S P Vyas
Journal: Drug delivery (0)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: YIGSR peptide; pegylated nanospheres; 5-fluorouracil; angiogenic endothelial cells; laminin receptors
Affiliations: Novel Drug Delivery Systems Laboratory, Strides Arcolab Limited, Bangalore, Karnataka, 560076, India. 

Abstract:  YIGSR peptide anchored pegylated nanospheres (YIGSR-SN) loaded with 5-fluorouracil (5-FU) were investigated for selective and preferential presentation of carrier contents at angiogenic endothelial cells over-expressing laminin receptors on and around tumor tissue and thus for assessing their targetability. Pegylated nanosphere (SN) without peptide conjugate were used for comparison. The average size of all nanosphere preparations prepared was approximately 108 nm and maximum drug entrapment was 68.5 +/- 5.2%. In vitro endothelial cell binding of nanospheres exhibited 8-fold higher binding of YIGSR-SN to HUVEC in comparison to the SN. Spontaneous lung metastasis and angiogenesis assays show that YIGSR peptide anchored nanospheres are significantly (p &lt;or= 0.05) effective in the prevention of lung metastasis and angiogenesis compared to free 5-FU and SN. In therapeutic experiments, 5-FU, SN, and YIGSR-SN were administered intravenously on day 4 at the dose of 10 mg 5-FU/kg body weight to B16F10 tumor bearing BALB/c mice resulting in effective regression of tumors in YIGSR-SN compared with free 5-FU and SN. Results indicate that YIGSR peptide anchored pegylated nanospheres bearing 5-FU are significantly (p &lt;or= 0.05) active against primary tumor and metastasis than the non-targeted pegylated nanospheres and free drug. Thus, YIGSR peptide anchored pegylated nanospheres hold potential of targeted cancer chemotherapeutics. 

Retracted: No

PubPeer comments:
 Right: Figure 2.  Transmission electron microscopic image of YIGSR modified albumin nanoparticles (YIGSR-SN). Left: Figure 3 from [Mishra et al (2006)] .  Transmission electron microscopic image of transferrin modified albumin nanoparticles (Tf-PEG-NPs) ![file] Were the NPs modified with transferrin, for targeted brain delivery of AZT, or with YIGSR peptide, for tumor targeting? ,
Cisplatin induces apoptosis of A549 cells by downregulating peroxidase V
Authors: X Chen
K-W Wang
Y-Q Chen
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cisplatin; apoptosis; A549 cells; peroxidase V; downregulating
Affiliations: Medical College, Shandong University, Jinan, China.

Abstract:  The article "Cisplatin induces apoptosis of A549 cells by downregulating peroxidase V" by X. Chen, K.-W. Wang, Y.-Q. Chen, published in Eur Rev Med Pharmacol Sci 2018; 22(21): 7289-7295 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
Identification of a novel complex between human kallikrein 2 and protease inhibitor-6 in prostate cancer tissue
Authors: S D Mikolajczyk
R L Wolfert
D J Tindall
K M Marker
M C Charlesworth
L S Marks
H G Rittenhouse
L S Millar
Journal: Cancer Research (1999)
Discipline: CLINICAL MEDICINE
Keywords: hK2; serine protease; prostate; protease inhibitor-6; PI-6
Affiliations: Hybritech Inc., San Diego, California 92121, USA. 

Abstract:  Human kallikrein (hK) 2 is an arginine-selective serine protease expressed predominantly in the prostate that has an 80% sequence identity with prostate-specific antigen. Expression of hK2 is elevated in the tumor epithelium compared to benign prostate tissue. We have purified, sequenced, and identified a novel hK2 complex in prostate tissue consisting of hK2 and a serine protease inhibitor known as protease inhibitor-6 (PI-6). This 64-kDa SDS-PAGE stable complex is elevated in the tumor and is approximately 10% of total hK2. No comparable complex of prostate-specific antigen was detected. PI-6, also known as cytoplasmic antiprotease, has been characterized as an intracellular inhibitor of trypsin and chymotrypsin-like proteases, which has high homology to plasminogen activator inhibitor 1 and 2. The physiological role of PI-6 in the prostate and its relationship to hK2 and prostate cancer are under investigation. 

Retracted: No

PubPeer comments:
 Figure 2. Vertical and horizontal, abrupt changes in signal. https: imgur.com NADlbWz ,
Accumulation of synovial fluid CD19+CD24hiCD27+ B cells was associated with bone destruction in rheumatoid arthritis
Authors: Ming Li
Chongling Sun
Jing Zheng
Xiaofeng Guo
Xiangjun Cui
Shulin Song
Huifang Zhang
Hongjiang Liu
Ke Zheng
Tingting Xu
Min Su
Kai Wang
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Regulatory B cells; CD19+CD24hiCD27+; Rheumatoid arthritis; Synovial fluid; Bone destruction
Affiliations: Department of Rheumatology and Immunology, The People's Hospital of China Three Gorges University/The First People's Hospital of Yichang, No. 4, Hudi Street, Xiling District, Yichang, 443000, Hubei Province, China., Department of Hematology, The People's Hospital of China Three Gorges University/The First People's Hospital of Yichang, Yichang, 443000, Hubei Province, China., Department of Rheumatology and Immunology, The People's Hospital of China Three Gorges University/The First People's Hospital of Yichang, No. 4, Hudi Street, Xiling District, Yichang, 443000, Hubei Province, China. .

Abstract:  Regulatory CD19+CD24hiCD27+ B cells were proved to be numerically decreased and functionally impaired in the peripheral blood (PB) from rheumatoid arthritis (RA), with the potential of converting into osteoclast-priming cells. However, the distribution and function of CD19+CD24hiCD27+ B cells in RA synovial fluid (SF) were unclear. In this study, we investigated whether RA SF CD19+CD24hiCD27+ B cells were increased and associated with bone destruction. We found that the proportion of RA SF CD19+CD24hiCD27+ B cells was increased significantly, and was positively correlated with swollen joint counts, tender joint counts and disease activity. CXCL12, CXCL13, CCL19 contributed to the recruitment of CD19+CD24hiCD27+ B cells in RA SF. Notably, CD19+CD24hiCD27+ B cells in the SF from RA expressed significantly more RANKL compared to OA and that in the PB from RA. Critically, RA CD19+CD24hiCD27+ B cells promoted osteoclast (OC) differentiation in vitro, and the number of OCs was higher in cultures with RA SF CD19+CD24hiCD27+ B cells than in those derived from RA PB. Collectively, these findings revealed the accumulation of CD19+CD24hiCD27+ B cells in SF and their likely contribution to joint destruction in RA. Modulating the status of CD19+CD24hiCD27+ B cells might provide novel therapeutic strategies for RA. 

Retracted: No

PubPeer comments:
 In Figure 4A, the patterns of the 2nd and 4th flow panel look almost identical. Panel 2 looks like it has more cells in the boxed region, but the plot of cells below that is identical to the flow plot in the 4th panel. https: media.springernature.com full springer-static image art%3A10.1038%2Fs41598-020-71362-7 MediaObjects 41598_2020_71362_Fig4_HTML.png?as=webp , 
 Thanks for the comments. The representative flow cytometry plot of the 2nd and 4th was from the same OA SF. The 4th flow panel is a Fluorescence-minus-one (FMO) control used to determine positive negative boundaries. ,
Long non-coding RNA H19 aggravates keloid progression by upregulating SMAD family member 5 expression via miR-196b-5p
Authors: Huiming Wei
Cheng Gong
Zhichao Li
Journal: Bioengineered (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: keloid; lncRNA H19; miR-196b-5p; smad5.
Affiliations: Department of Hand and Foot Microsurgery, Hanyang Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, Hubei, China, Department of Dermatological, Huazhong University of Science and Technology and Jiangbei Hospital, Wuhan, Hubei, China, Department of Medical and Beauty, Huazhong University of Science and Technology and Jiangbei Hospital, Wuhan, Hubei, China

Abstract:  Accumulating evidence suggests that long non-coding RNAs (lncRNAs) participate in the formation and development of keloids, a benign tumor. In addition, lncRNA H19 has been shown to act on the biological processes of keloids. This study aimed to identify other important mechanisms of the effect of lncRNA H19 on keloid formation. The H19, miR-196b-5p, and SMAD family member 5 (SMAD5) expression levels were detected using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western blotting. Subcellular localization of lncRNA H19 was detected using a nuclear-cytoplasmic separation assay. Cell viability and proliferation were measured using counting kit-8 and colony formation assays. Bax and Bcl-2 levels were examined using Western blot analysis. The interaction between H19 and miR-196b-5p or SMAD5 was verified using a dual-luciferase reporter assay. H19 and SMAD5 expression was upregulated in keloid tissue and fibroblasts, whereas miR-196b-5p expression was downregulated. Knockdown of H19, overexpression of miR-196b-5p, or knockdown of SMAD5 inhibited the viability and proliferation of keloid fibroblasts and promoted apoptosis. Overexpression of H19 or SMAD5 and knockdown of miR-196b-5p promoted viability and proliferation and inhibited apoptosis. miR-196b-5p was identified as a H19 sponge, and SMAD5 was identified as a miR-196b-5p target. The combination of lncRNA H19 and miR-196b-5p regulates SMAD5 expression and promotes keloid formation, thus providing a new direction for keloid treatment. 

Retracted: No

PubPeer comments:
 Can the authors please provide more details regarding the patients included in this study (approval number, time periode for sample collection)? Three of the PCR primers listed in Table 1 appear to be incorrect. The cell viability presentation in Figure 6b is hard to understand. What is on the y-axis? It looks like all the cells are almost dead and then start to live. Why is not the funding information available? I see no reason to hide this information. ![file] ,
pp90RSK- and protein kinase C-dependent pathway regulates p42/44MAPK-induced LDL receptor transcription in HepG2 cells
Authors: Gurpreet S Kapoor
Kamal D Mehta
Carmen Golden
Brett Atkins
Journal: Journal of lipid research (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Raf/MEK/p42/44MAPK cascade; LDL receptor expression; HepG2-Delta Raf-1:ER cells; Sp1; SRE-1
Affiliations: Department of Molecular and Cellular Biochemistry, The Ohio State University College of Medicine and Public Health, 464 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210, USA. 

Abstract:  We have previously shown that different extracellular stimuli require signaling through the Raf/MEK/p42/44MAPK cascade to induce LDL receptor expression. The present studies were designed to delineate the molecular mechanisms underlying p42/44MAPK-induced LDL receptor transcription in HepG2-Delta Raf-1:ER cells, a modified HepG2 cell line in which the Raf-1/MEK/p42/44MAPK cascade can be specifically activated by anti-estradiol ICI182,780 in an agonist-specific manner. Using these cells, we show that: a) LDL receptor induction was reduced in reporter constructs containing mutation in either Sp1 or sterol-regulatory element-1 (SRE-1) sites, whereas inactivation of both sites abolished the induction; b) E1A, which inhibits CREB binding protein (CBP), a common activator of SRE-1 binding protein and Sp1, strongly repressed the induction; c) intracellular inhibition of the 90 kDa ribosomal S6 kinase (pp90RSK) cascade reduced LDL receptor induction; d) highly selective protein kinase C (PKC) inhibitors effectively abrogated the induction without affecting activation of pp90RSK; and e) overexpression of PKC beta significantly induced LDL receptor promoter activity. Taken together, these results demonstrate that pp90RSK and PKC beta are downstream effectors and Sp1, SRE-1 binding protein, and CBP are part of the transcriptional complex resulting in induction of LDL receptor expression in response to activation of the Raf/MEK/p42/44MAPK cascade. These findings identify for the first time a role for PKC beta in determining the specificity of p42/44MAPK signaling by participating with pp90RSK in regulating gene expression. 

Retracted: No

PubPeer comments:
 Figures 5A and 5C. Much more similar than expected. https: imgur.com nOsIHXL , 
 Figure 5. Much more similar and different than expected. https: imgur.com OqyCozd ,
Translocation of full-length Bid to mitochondria during anoikis
Authors: Andrew P Gilmore
Anthony J Valentijn
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Epithelial cells; adhesion; extracellular matrix; apoptosis; anoikis
Affiliations: Wellcome Trust Centre for Cell Matrix Research, School of Biological Sciences, Manchester University, Manchester M13 9PT, United Kingdom.

Abstract:  Epithelial cells require adhesion to the extracellular matrix for survival, and in the absence of adhesion they undergo apoptosis (anoikis). This is distinct from apoptosis induced by extracellular death ligands, such as tumor necrosis factor, which result in direct activation of caspase 8. Bid is a member of the BH3-only subfamily of the Bcl-2 proteins and is important for most cell types to apoptose in response to Fas and tumor necrosis factor receptor activation. Caspase 8 cleaves full-length Bid, resulting in truncated p15 tBid. p15 tBid is potently apoptotic and activates the multidomain Bcl-2 protein, Bax, resulting in release of cytochrome c from mitochondria. We have previously shown that Bax rapidly translocates from the cytosol to mitochondria following loss of adhesion and that this is required for anoikis. We have now examined the role of Bid in anoikis. Bid translocates to mitochondria with identical kinetics as Bax. Although Bid is required for anoikis, it does not require proteolytic cleavage by caspase 8. Furthermore, it does not require Bid to interact directly with other Bcl-2 family proteins, such as Bax. Our data indicate that Bid is important for regulating apoptosis via the intrinsic pathway and has implications for how Bid may fulfill that role. 

Retracted: No

PubPeer comments:
 Unexpectedly similar bands, and undeclared spicing, in Fig. 3a. ![file] ,
Estrogen receptor alpha, a molecular switch converting transforming growth factor-alpha-mediated proliferation into differentiation in neuroblastoma cells
Authors: Serena Ghisletti
Paola Mussi
Ivano Eberini
Paolo Ciana
Adriana Maggi
Elisabetta Vegeto
Journal: Journal of Biological Chemistry (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Transforming growth factor-alpha; neural cell progenitors; estrogen receptor-alpha; SK-N-BE; mitogenic signaling
Affiliations: Center of Excellence on Neurodegenerative Diseases, University of Milan, 20133 Milan, Italy.

Abstract:  Transforming growth factor-alpha (TGF-alpha) is known to promote both proliferation and differentiation of neural cell progenitors. Using the human neuroblastoma cell line SK-N-BE that is induced to proliferate by TGF-alpha, we demonstrated that the expression of a single transcription factor, the estrogen receptor-alpha (ER alpha), can reroute the TGF-alpha mitogenic signaling toward a path leading to differentiation. With selected mutations in ER alpha and signal transducer and activator of transcription 3 (Stat3), we demonstrated that the blockade of TGF-alpha mitotic potential was not dependent on ER alpha DNA binding activity but required a transcriptionally active Stat3. In neuroblastoma cells, 17 beta-estradiol treatment induced a transient increase in the transcription of estrogen-responsive element-containing promoters including those regulating TGF-alpha and prothymosin alpha synthesis. Based on the data presented, we hypothesized that in the presence of prothymosin alpha, ER alpha activates its direct target genes and increases cell proliferation, whereas in the presence of high levels of TGF-alpha, ER alpha preferentially interacts with Stat3 and causes cell differentiation. Our results reveal a novel form of "end-product" regulation of an intracellular receptor that occurs through recruitment of membrane receptors and their signaling effector system. Cross-coupling between membrane and intracellular receptors has been described by several laboratories. This study proves the relevance of these interactions in cellular responses to growth factors. 

Retracted: No

PubPeer comments:
 ![file] ,
Cross-talk between the survival kinases during early reperfusion: its contribution to ischemic preconditioning
Authors: Derek M Yellon
Derek J Hausenloy
Mihaela M Mocanu
Journal: Cardiovascular Research (2004)
Discipline: CLINICAL MEDICINE
Keywords: Survival kinase cascades; PI3K-Akt; Raf-MEK1/2-Erk1/2; ischemic preconditioning; 'cross-talk'
Affiliations: The Hatter Institute and Centre for Cardiology, University College London Hospital, and Medical School, Grafton Way, London WC1E 6DB, UK.

Abstract:  Objectives: Recruitment of the survival kinase cascades, PI3K-Akt and Raf-MEK1/2-Erk1/2, at the time of reperfusion, following a lethal ischemic insult, may mediate the protection associated with ischemic preconditioning (IPC). The exact interplay between these two kinase cascades in mediating this effect is not clear. We examine the 'cross-talk' between these kinase cascades in their contribution to IPC-induced protection. Methods and results: In isolated perfused rat hearts subjected to 35 min of lethal ischemia +/- ischemic preconditioning, the phosphorylation states of Akt, Erk1/2, p70S6K were determined after 15 min of reperfusion, and infarct size was measured after 120 min of reperfusion. IPC induced a threefold increase in Akt, Erk1/2, and p70S6K phosphorylation, at reperfusion. We found that inhibiting the PI3K-Akt (using LY294008) at reperfusion induced the phosphorylation of Erk1/2-p70S6K, and conversely, that inhibiting the MEK1/2-Erk1/2 pathway (using PD 98059) at reperfusion, induced the phosphorylation of Akt, suggesting 'cross-talk' between the two kinase pathways. However, this effect was not accompanied by a reduction in infarct size (43.1 +/- 7.2% with LY 294008 and 57.7 +/- 7.0% with PD 98059 vs. 46.3 +/- 5.8% in control; P = NS), suggesting that both the kinase cascades may need to be activated to mediate IPC-induced protection. IPC reduced the infarct-risk volume ratio to 17.8 +/- 2.3% from 46.3 +/- 5.8% in control (P &lt; 0.01). Inhibiting p70S6K, a kinase situated downstream of both PI3K and Erk1/2, using rapamycin, abolished IPC-induced protection (46.0 +/- 7.7% with IPC+RAPA vs. 17.8 +/- 2.3% with IPC; P &lt; 0.01). Conclusions: We report that, the survival kinase cascades PI3K-Akt and MEK1/2-Erk1/2, which are recruited at the time of reperfusion in response to ischemic preconditioning, exhibit 'cross-talk' such that inhibiting one cascade activates the other and vice versa. Furthermore, at the time of reperfusion, these kinase cascades mediate IPC-induced protection, by acting in concert via p70S6K. 

Retracted: No

PubPeer comments:
 Hi All: For Figure 3a: the WB image of IPC+PD looks very strange. Is this considered as manipulating WB result? thanks Peer ,
Visual detection of melamine in milk samples based on label-free and labeled gold nanoparticles
Authors: Zhihong Liu
Philip Tinnefeld
Qiao Ma
Hui Huang
Guohua Zhou
Guoping Zeng
Yuqi Feng
Zhike He
Li Li
Journal: Talanta (2011)
Discipline: CHEMISTRY
Keywords: Melamine; polythymine; hydrogen bonding; colorimetric detection; gold nanoparticles
Affiliations: Key Laboratory of Analytical Chemistry for Biology and Medicine (Ministry of Education), College of Chemistry and Molecular Sciences, Wuhan University, Wuhan 430072, China.

Abstract:  Melamine that can cause serious damage to the organs of animal or human beings was found to bind to polythymine via hydrogen bonding. With this novel discovery, colorimetric detection of melamine based on label-free and labeled gold nanoparticles was developed, respectively. Both of the methods revealed good selectivity for melamine over other components that may exist in milk and good anti-influence ability. The raw milk samples were pretreated according to the National standard method combined with a solid phase extraction monolithic column. The accurate quantification of melamine as low as 41.7 nM and 46.5 nM was obtained, respectively. It also guarantees fast and reliable readout with naked eyes, making visual detection possible. Further comparison between label-free and labeled based methods was discussed in this paper. 

Retracted: No

PubPeer comments:
 The same micrograph has been used three times in Figure 3a and 5a,b, but presented as different. In addition, the micrograph in Figure 3b and 5c can be anything. ![file] ,
Circ-ABCB10 promotes proliferation and invasion of esophageal squamous cell carcinoma cells by modulating microRNA-670-3p
Authors: Y-X Pei
K-Q Liu
J Tan
J-B Ma
J Zhao
W-Q Zhang
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: circ-ABCB10; esophageal squamous cell carcinoma; oncogene; tumors; biological function
Affiliations: Department of Thoracic Surgery, the 7th Medical Center of PLA General Hospital, Beijing, China. .

Abstract:  Objective: Circ-ABCB10 is a non-coding RNA newly discovered in recent years. It has been observed to serve as an oncogene in a variety of tumors, but its biological function in esophageal squamous cell carcinoma (ESCC) is still unknown. The purpose of this study was to investigate the circ-ABCB10 expression in ESCC and its possible molecular mechanism. Patients and methods: Circ-ABCB10 expression in ESCC tissue samples and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The impacts of circ-ABCB10 on the biological functions of ESCC cells were examined by cell counting kit-8 (CCK-8) and transwell assays. Moreover, bioinformatics analysis was used to determine the binding sites between miRNAs and circ-ABCB10, and the binding relationship was verified by qRT-PCR and Luciferase assay. Results: QRT-PCR analysis revealed that circ-ABCB10 expression in both ESCC tissues and cell lines was higher than that in the normal control group. Patients in high TNM stage exhibited a higher expression of circ-ABCB10 than those in low stage, and this high expression predicted a poor prognosis of ESCC patients. Inhibiting circ-ABCB10 expression remarkably inhibited the growth and metastasis of ESCC cells. In addition, it was demonstrated that circ-ABCB10 could bind to microRNA-670-3p and inhibit its expression. Downregulation of microRNA-670-3p partially reversed the inhibitory impact of low-expressing circ-ABCB10 on cell growth and migration rate. Conclusions: Circ-ABCB10 accelerates the metastasis and proliferation of ESCC cells by binding to microRNA-670-3p. This circ-ABCB10 / microRNA-670-3p axis may become a potential therapeutic target for ESCC therapy. 

Retracted: No

PubPeer comments:
  A total of 45 ESCC tumor tissues and 45 normal control tissues were collected from ESCC patients who underwent surgery in the 7th Medical Center of PLA General Hospital from **July 2017 to June 2019** . Fig 1C.  Highly expressed circ-ABCB10 was predictive of poor prognosis in ESCC patients. ![file] The authors followed their patients survival for nearly 5 years after recruitment, i.e. through the date range **mid-2022 to mid-2024**. ,
p14(ARF) inhibits the growth of lung adenocarcinoma cells harbouring an EGFR L858R mutation by activating a STAT3-dependent pro-apoptotic signalling pathway
Authors: S Gazzeri
D Dayde
B Eymin
P Ozenne
E Brambilla
Journal: Oncogene (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: EGFR; mutations; lung tumours; p14(ARF); apoptosis
Affiliations: Equipe Bases Moléculaires de la Progression des Cancers du Poumon, Centre de Recherche INSERM U823, Institut Albert Bonniot, Grenoble, France.

Abstract:  Epidermal growth factor receptor (EGFR) stimulates proliferative and survival signals. Activating mutations of EGFR are involved in the aetiology and maintenance of the malignant phenotype of lung tumours. We previously described the frequent association of these mutations with the decreased expression of the p14(ARF) tumour suppressor, another common feature of lung cancer. Based on these data, we postulated that p14(ARF) could protect cells against untimely or excessive mitotic signals induced by mutant EGFR. In this study, we demonstrate that p14(ARF) promotes apoptosis in lung tumour cells harbouring the EGFR L858R mutation through the accumulation of phosphorylated signal transducer and activator of transcription 3 (STAT3) on Tyr 705 residue, which leads to Bcl-2 downregulation. Using siRNA against PTP-RT, the phosphatase that specifically targets Tyr 705 residue, we show that accumulation of pSTAT3-Tyr705 promotes EGFR L858R mutant cell death, thereby confirming the existence of a STAT3-dependent pro-apoptotic pathway in these cells. Finally, we show that the expression of the EGFR L858R mutant represses p14(ARF) expression and inhibits STAT3/Bcl-2 signalling. These results identify a novel link between the p14(ARF) and EGFR pathways and suggest that EGFR L858R counteracts the pro-apoptotic function of p14(ARF) by downregulating its expression to promote carcinogenesis. 

Retracted: No

PubPeer comments:
 The same GAPDH controls have been used in Figure 2B (one Western blotting panel) and Figure 3B (both Western blotting panels). This may have implications for the reported protein quantification graphs. ,
Antiestrogenic Activity of Triptolide in Human Breast Cancer Cells MCF-7 and Immature Female Mouse
Authors: Jun Wang
Lijun Wang
Jinghua Cheng
Yi Tang
Journal: Drug development research (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MCF-7 cells; antiestrogenic activity; triptolide.
Affiliations: Department of Cardiology; Jinling Hospital, Nanjing University School of Medicine; Nanjing Jiangsu China

Abstract:  Preclinical Research To investigate the antiestrogenic activity of triptolide in human breast cancer cell line MCF-7 and immature female C57BL/6 mouse. The effects of triptolide on cell proliferation, cell cycle, and the expression of estrogen receptor alpha (ERα) and progesterone receptor (PR) were examined in MCF-7 cells. In vivo antiestrogenic effects of triptolide were observed after cotreatment of mice with E2 and triptolide for 4 days. Triptolide dose- and time-dependently inhibited cell growth in untreated or E2 -treated MCF-7 cells, which was associated with increased S phase arrest. Furthermore, triptolide down regulated the expression of ERα and PR in cells. The expression of ERα and PR in combined group of triptolide with E2 was much higher than that of triptolide alone. Triptolide decreased the E2 -induced uterine weight in mice, while triptolide alone had no effect. Triptolide treatment (90 μg/kg) resulted in extensive degeneration and necrosis of uterine epithelial cells, whereas the same concentration of triptolide in combination with E2 caused morphologic changes in epithelial cells from simple columnar to ellipse, without destruction. Triptolide showed antiestrogenic activity in vitro and in vivo, and the down regulation of ERα and PR expression may be its underlying mechanisms. Drug Dev Res 78 : 164-169, 2017. © 2017 Wiley Periodicals, Inc. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] , 
 Figure 5A. * Green boxes: the Stat1 panel in this figure looks similar to the Snail-1 panel in another paper by the same first author and research group. The dark red box is the one also marked above, just for orientation purposes. ![file] ,
MicroRNA-296 functions as a tumor suppressor in breast cancer by targeting FGFR1 and regulating the Wnt/β-catenin signaling pathway
Authors: D-M Zhu
Y Miao
W-M Sun
W Tao
J-C Li
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Breast cancer; MicroRNAs; miR-296; tumorigenesis; qRT-PCR
Affiliations: Department of General Surgery Breast Ward, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China. .

Abstract:  Objective: Breast cancer (BC) is a common malignancy all over the world. However, the detailed mechanism underlying BC progression remains incompletely understood. MicroRNAs (miRNAs) have been observed to play crucial roles in tumorigenesis. The present study aimed to determine the expression and function of miR-296 in BC. Patients and methods: MiR-296 expressions in BC tissue samples and cell lines were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). After that, we performed functional assays, including MTT (3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assays and transwell assays, to show the functions of miR-296 in BC cell proliferation, invasion and migration. Immunological histological chemistry (IHC) assays were carried out to detect the expression levels of fibroblast growth factor receptor 1 (FGFR1) in BC tissue samples. Western blot was used to explore potential mechanisms of miR-296 in regulating BC progression. A Luciferase reporter assay was carried out to confirm the target gene of miR-296. Results: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) results demonstrated a significant decrease of miR-296 expressions in BC when compared to the corresponding normal controls. In addition, the decreased miR-296 was correlated with the malignant phenotypes and poorer prognosis of BC patients. The functional assays indicated that miR-296 restoration could repress the proliferation, invasion and migration abilities of BC cells. Moreover, the results of the current study revealed that miR-296 exerted the repressive functions in BC cells via regulating FGFR1, the Wnt/β-catenin signaling pathway and EMT. Additionally, miR-296 up-regulation could inhibit in vivo BC cell growth. Conclusions: All these findings indicated that miR-296 exerted anti-BC functions, providing novel therapeutic strategies in BC treatment. 

Retracted: No

PubPeer comments:
 Image duplications with two other published papers from the same research group ![file] ![file] , 
 Figure 3 and Fig 4 have some similarities, though the histopathology sections were from the male (Fig. 3) and female (Fig. 4). ![file] , 
 Another published paper from the same research group has some unusual similarities with this paper. ![file] ![file] ,
PD-L1 blockade in combination with inhibition of MAPK oncogenic signaling in patients with advanced melanoma
Authors: Caroline Robert
Alain Algazi
Katie M Campbell
Sunandana Chandra
Donald Lawrence
Antoni Ribas
Michael Gordon
Jose Lutzky
Shannon Marshall
Marcus O Butler
Leonel Hernandez-Aya
Bruno Delafont
Wilson H Miller Jr
Paolo A Ascierto
Nancy Mueller
Journal: Nature Communications (2020)
Discipline: Multidisciplinary
Keywords: PD-L1 blockade; MAPK signaling; durvalumab; dabrafenib; trametinib
Affiliations: University of California Los Angeles (UCLA) and Jonsson Comprehensive Cancer Center at UCLA, Los Angeles, CA, USA. ., UCSF Medical Center, San Francisco, CA, USA., Istituto Nazionale Tumori IRCCS Fondazione Pascale, Naples, Italy., Princess Margaret Cancer Centre, Toronto, ON, Canada., Northwestern Memorial Hospital, Chicago, IL, USA., HonorHealth Research Institute, Scottsdale, AZ, USA., Washington University School of Medicine, St. Louis, MO, USA., Massachusetts General Hospital, Boston, MA, USA., Mount Sinai Medical Center, Miami Beach, FL, USA., Segal Cancer Center, Jewish General Hospital, Rossy Cancer Network, McGill University, Montreal, QC, Canada., University of California Los Angeles (UCLA) and Jonsson Comprehensive Cancer Center at UCLA, Los Angeles, CA, USA., AstraZeneca, Gaithersburg, MD, USA., Gustave Roussy Cancer Campus and Paris-Saclay University, Villejuif, France.

Abstract:  Combining PD-L1 blockade with inhibition of oncogenic mitogen-activated protein kinase (MAPK) signaling may result in long-lasting responses in patients with advanced melanoma. This phase 1, open-label, dose-escalation and -expansion study (NCT02027961) investigated safety, tolerability and preliminary efficacy of durvalumab (anti-PD-L1) combined with dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) for patients with BRAF-mutated melanoma (cohort A, n = 26), or durvalumab and trametinib given concomitantly (cohort B, n = 20) or sequentially (cohort C, n = 22) for patients with BRAF-wild type melanoma. Adverse events and treatment discontinuation rates were more common than previously reported for these agents given as monotherapy. Objective responses were observed in 69.2% (cohort A), 20.0% (cohort B) and 31.8% (cohort C) of patients, with evidence of improved tumor immune infiltration and durable responses in a subset of patients with available biopsy samples. In conclusion, combined MAPK inhibition and anti-PD-L1 therapy may provide treatment options for patients with advanced melanoma. 

Retracted: No

PubPeer comments:
 Possible differential splicing. Could authors check it provide the raw data please? Figure 2D: ![file] Figure 4C: ![file] , 
 Supplemental Fig. 1: More similar than expected. Could authors check please? ![file] , 
 There may also be a splice in the first band. *** ![file] , 
 Fig. 1F: Possible differential splicing. Could authors check it provide the raw data please? ![file] ,
Honokiol inhibits non-small cell lung cancer cell migration by targeting PGE₂-mediated activation of β-catenin signaling
Authors: Tripti Singh
Santosh K Katiyar
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Lung cancer; honokiol; non-small cell lung cancer; cell migration; COX-2
Affiliations: Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.

Abstract:  Lung cancer remains a leading cause of death due to its metastasis to distant organs. We have examined the effect of honokiol, a bioactive constituent from the Magnolia plant, on human non-small cell lung cancer (NSCLC) cell migration and the molecular mechanisms underlying this effect. Using an in vitro cell migration assay, we found that treatment of A549, H1299, H460 and H226 NSCLC cells with honokiol resulted in inhibition of migration of these cells in a dose-dependent manner, which was associated with a reduction in the levels of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2). Celecoxib, a COX-2 inhibitor, also inhibited cell migration. Honokiol inhibited PGE2-enhanced migration of NSCLC cells, inhibited the activation of NF-κB/p65, an upstream regulator of COX-2, in A549 and H1299 cells, and treatment of cells with caffeic acid phenethyl ester, an inhibitor of NF-κB, also inhibited migration of NSCLC cells. PGE2 has been shown to activate β-catenin signaling, which contributes to cancer cell migration. Therefore, we checked the effect of honokiol on β-catenin signaling. It was observed that treatment of NSCLC cells with honokiol degraded cytosolic β-catenin, reduced nuclear accumulation of β-catenin and down-regulated matrix metalloproteinase (MMP)-2 and MMP-9, which are the down-stream targets of β-catenin and play a crucial role in cancer cell metastasis. Honokiol enhanced: (i) the levels of casein kinase-1α, glycogen synthase kinase-3β, and (ii) phosphorylation of β-catenin on critical residues Ser(45), Ser(33/37) and Thr(41). These events play important roles in degradation or inactivation of β-catenin. Treatment of celecoxib also reduced nuclear accumulation of β-catenin in NSCLC cells. FH535, an inhibitor of Wnt/β-catenin pathway, inhibited PGE2-enhanced cell migration of A549 and H1299 cells. These results indicate that honokiol inhibits non-small cell lung cancer cells migration by targeting PGE2-mediated activation of β-catenin signaling. 

Retracted: No

PubPeer comments:
 Figure 2C. * Blue boxes: Two panels appear to look similar to each other. This was reported to the journal in 2015, with a friendly reminder in 2016, but no response so far. ![file] , 
 https: retractionwatch.com 2019 01 07 former-uab-natural-products-researcher-up-to-a-dozen-retractions ,
MiR-221 inhibits proliferation of pancreatic cancer cells via down regulation of SOCS3
Authors: H-H Cheng
X-J Xue
J-T Wen
J Xie
X-Z Wang
K-P Zhang
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: JAK-STAT pathway; SOCS3; miR-221; pancreatic cancer; proliferation
Affiliations: Department of Radiotherapy, Xingtai People's Hospital, Xingtai, Hubei, China. .

Abstract:  Objective: The over-activation of Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway induced by cytokines are closely correlated with tumorigenesis. Suppressor of cytokine signaling 3 (SOCS3) serves as a negative regulator for JAK-STAT, and its down-regulation is involved in the oncogenesis of pancreatic cancer. We aimed at investigating the effect of miR-221 on the expression and proliferation, cycle and apoptosis of pancreatic cancer cells and determine the related mechanism. Patients and methods: Dual luciferase reporter gene assay was used to analyze the regulation between miR-221 and SOCS3. The expressions of miR-221, SOCS3, p-JAK and p-STAT3 in normal human pancreatic epithelial cell HPDE6-C7 and pancreatic cancer cell PANC-1 were quantified by qPCR and Western blot. Flow cytometry was used to identify cell cycle and proliferation. In vitro cultured PANC-1 cells were transfected with miR-221 inhibitor or pIRES2-SOCS3. The expressions of miR-221, SOCS3, p-JAK and p-STAT3, along with the cell proliferation or apoptosis, were compared. Results: Bioinformatics analysis showed the existence of binding site between miR-221 and 3'-UTR of SOCS3 mRNA. Dual luciferase gene reporter assay confirmed the targeted regulation between miR-221 and SOCS3. Compared to HPDE6-C7 cells, higher levels of miR-221, p-JAK and p-STAT3 expression, and lower expression of SOCS3, were found in PANC-1 cells, along with the increase of cell proliferation. Transfection of miR-221 inhibitor or pIRES2-SOCS3 remarkably enhanced SOCS3 expression, inhibited the levels of p-JAK and p-STAT3 expression, and impeded the proliferation of PANC-1 cells. Conclusions: MiR-221 decreases proliferation potency of PANC-1 cells and affects JAK-STAT3 signaling pathway via inhibiting SOCS3. 

Retracted: No

PubPeer comments:
 Figure 7B. Much more similar after horizontal flip than expected. ![file] ,
GADD45-induced cell cycle G2-M arrest associates with altered subcellular distribution of cyclin B1 and is independent of p38 kinase activity
Authors: Shunqian Jin
Baskaran Rajasekaran
Lucia Mazzacurati
Xianxing Li
Tong Tong
Feiyue Fan
Kimberly L Petrik
Min Wu
Xiaocheng Zhu
Wenhong Fan
Qimin Zhan
Michael J Antinore
Journal: Oncogene (2002)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DNA damage; cell cycle checkpoint; Gadd45; G2-M checkpoint; p53-regulated
Affiliations: Department of Radiation Oncology, Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, PA 15213, USA.

Abstract:  In response to DNA damage, the cell cycle checkpoint is an important biological event in maintaining genomic fidelity. Gadd45, a p53-regulated and DNA damage inducible protein, has recently been demonstrated to play a role in the G2-M checkpoint in response to DNA damage. In the current study, we further investigated the biochemical mechanism(s) involved in the GADD45-activated cell cycle G2-M arrest. Using the tetracycline-controlled system (tet-off), we established GADD45-inducible lines in HCT116 (wild-type p53) and Hela (inactivated p53 status) cells. Following inducible expression of the Gadd45 protein, cell growth was strongly suppressed in both HCT116 and Hela cells. Interestingly, HCT116 cells revealed a significant G2-M arrest but Hela cells failed to arrest at the G2-M phases, indicating that the GADD45-activated G2-M arrest requires normal p53 function. The GADD45-induced G2-M arrest was observed independent of p38 kinase activity. Importantly, induction of Gadd45 protein resulted in a reduction of nuclear cyclin B1 protein, whose nuclear localization is critical for the completion of G2-M transition. The reduced nuclear cyclin B1 levels correlated with inhibition of Cdc2/cyclin B1 kinase activity. Additionally, overexpression of cyclin B1 substantially abrogated the GADD45-induced cell growth suppression. Therefore, GADD45 inhibition of Cdc2 kinase activity through alteration of cyclin B1 subcellular localization may be an essential step in the GADD45-induced cell cycle G2-M arrest and growth suppression. 

Retracted: No

PubPeer comments:
 There appears to be a mistake in the Figures in this paper. Figure 1 presents data from a two-way interaction between testing time and daily WMD use on anxiety. Figure 2 presents data from a three-way interaction between testing time, daily WMD use, and condition, on anxiety. As would be expected, the data-points in Figure 1 appear to be the average of the respective data-points in the two parts of Figure 2. However, at Time 3 for the High Daily WMD Users, the value in Figure 1 (approximately 40.4) is not the average of the respective values in Figure 2 (which are both approximately 42.2). The attached figures, in which the relevant values are highlighted, should clarify the problem. I wonder if one of the parts of Figure 2 was created from the other, but whoever did this forgot to change the value for Time 3 High Daily WMD Users. ![file] ![file] ,