PReD-Bench/PRed-Bench huggingface dataset:
LncRNA MALAT1 promotes cell proliferation and imatinib resistance by sponging miR-328 in chronic myelogenous leukemia
Authors: Zhong-Wei Lu
Yi-Xiong Cao
Feng Wen
Ze-Yu Luo
Pei Liao
Journal: Biochemical and biophysical research communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Chronic myeloid leukemia; Imatinib resistance; LncRNA MALAT1; Proliferation; miR-328.
Affiliations: Department of Hematology, The First Affiliated Hospital of University of South China, Hengyang, 421001, PR China. Electronic address: ., Department of Hematology, The First Affiliated Hospital of University of South China, Hengyang, 421001, PR China.

Abstract:  Background: Chronic myeloid leukemia (CML) is a type of cancer that starts in certain blood-forming cells of the bone marrow. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a well known protooncogene, has be shown to be upregulated in various tumor types, including multiple myeloma. However, the biological function of MALAT1 in CML remains has yet to be explored. This study was designed to investigate the effects of MALAT1 on the physiological processes in CML and its underlying mechanisms, which will be helpful for us to have a better understanding of CML development and progression as well as improved therapeutic method. Methods: Recombinant virus construction and infection was performed to overexpress or knockdown the expression of MALAT1. Dual luciferase reporter assay was applied to vetify the interaction between MALAT1 and miR-328. The cell viability and cell cycle were analyzed by CCK-8 assay and flow cytometry, respectively. Quantitative real time PCR and western blotting assays were used to measure the expression of genes and proteins. Results: The expression of MALAT1 was significantly increased in CML cells compared with peripheral blood cells from health donors. Silencing of MALAT1 significantly inhibited the proliferation and arrested cell cycle of CML cells by targeting miR-328. Moreover, MALAT1 knockdown enhanced imatinib sensitivity of K562 cells, while silencing of miR-328 abolished this effect. Conclusions: These findings indicate that lncRNA MALAT1/miR-328 axis promotes the proliferation and imatinib resistance of CML cells, providing new perspectives for the future study of MALAT1 as a therapeutic target for CML. 

Retracted: No

PubPeer comments:
 Figure 3 in this paper shows unexpected similarities to Figure 4 in an older paper by this group, i.e. * Arun Chauhan et al. Fungus-mediated biological synthesis of gold nanoparticles: potential in detection of liver cancer - International Journal of Nanomedicine 2011:6 2305u20132319 - DOI: 10.2147 IJN.S23195 Figure 3 in PLOS ONE 2012 (this paper) shows Atomic Force Microscopy analysis of 5-fluorouracil nano-particles synthesized by using Aloe vera leaf extract. Figure 4 in the IJN 2011 paper shows Atomic Force Microscopy analysis of gold nano-particles synthesized by using Candida albicans yeast extract. The 2D and 3D AFM images from both papers look unexpectedly similar. Marked here with red and blue boxes. ![file] ,
Elevated dopamine D2 receptor in prefrontal cortex of CUMS rats is associated with downregulated cAMP-independent signaling pathway
Authors: Ting-juan Xu
Cheng Chen
Wei-ping Xu
Jing-mo Yang
Ting-ting Hu
Wei Wei
Journal: Canadian Journal of Physiology and Pharmacology (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: depression; dopaminergic receptors; chronic stress; rat model; dopamine D2 receptors
Affiliations: Institute of Clinical Pharmacology of Anhui Medical University, Key Laboratory of Anti-inflammatory and Immunopharmacology of Education Ministry, Hefei 230032, Anhui, China., Anhui Provincial Hospital, Hefei 230001, Anhui, China.

Abstract:  Because depression is associated with significant morbidity and functional disability, it is important to reveal the mechanism of action. A variety of studies have suggested the involvement of dopaminergic receptors in the pathophysiological mechanism of non-stress-associated depression-like behavior in rodents. Nevertheless, controversy exists about whether chronic stress acts on dopaminergic receptors in the prefrontal cortex. Thus, we investigated the level of dopamine D2 receptors (DRD2) and the possible mechanisms involved in a chronic unpredictable mild stress (CUMS) rat model of depression. The results showed CUMS-induced, depression-like symptoms in the rat, characterized by reduced sucrose consumption and body mass, and increased duration of immobility in a forced swimming test. Moreover, chronic stress upregulated the expression of DRD2 but downregulated protein kinase A (PKA), transcription factor cAMP response element binding protein (CREB), and phospho-CREB (p-CREB) in the prefrontal cortex, as demonstrated by Western blot. Notably, in the rat model of depression, decreased cyclic adenine monophosphate (cAMP) levels and PKA activity were present at the same time, which is consistent with clinical findings in depressed patients. Our findings suggested that dopaminergic system dysfunction could play a central role in stress-related disorders such as depression. 

Retracted: No

PubPeer comments:
 The western blots in this manuscript appear weird with backgrounds and resolutions changing wildly within what is ostensibly the same blot. These blots in Figure 5 are, for example, obviously not from the same scan. ![file] The backgrounds for the two rows of blots are wholly incompatible. Did the authors massively change the exposure for the loading controls (beta-actin)? And why? Could the authors perhaps upload uncropped blots? , 
 Dear Coniochaeta Malacotricha, Thank you for your comment. We will investigate this question and reply you as soon as possible. Thank you for your heip again. Best regards ,
Type I and III interferons disrupt lung epithelial repair during recovery from viral infection
Authors: Hans Henrik Gad
Simon L Priestnall
Rune Hartmann
Jack Major
Stefania Crotta
Teresa M McCabe
Miriam Llorian
Andreas Wack
Journal: Science (2020)
Discipline: Multidisciplinary
Keywords: Cytokine signaling; Lung tissue damage; Respiratory viral infection; Type I interferons; Type III interferons
Affiliations: Immunoregulation Laboratory, The Francis Crick Institute, London, UK., Bioinformatics and Biostatistics, The Francis Crick Institute, London, UK., Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark., Department of Pathobiology and Population Sciences, The Royal Veterinary College, Hatfield, UK., Experimental Histopathology Science Technology Platform, The Francis Crick Institute, London, UK.

Abstract:  Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-α and IFN-β) and III (IFN-λ) interferons are host-produced antiviral cytokines. Prolonged IFN-α and IFN-β responses can lead to harmful proinflammatory effects, whereas IFN-λ mainly signals in epithelia, thereby inducing localized antiviral immunity. In this work, we show that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-λ driving these effects most potently. IFN-induced protein p53 directly reduces epithelial proliferation and differentiation, which increases disease severity and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN production aggravates viral infection by impairing lung epithelial regeneration. Timing and duration are therefore critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disease 2019 (COVID-19). 

Retracted: No

PubPeer comments:
 The  IFN-induced p53 directly reduces epithelial proliferation and differentiation, increasing disease severity, and susceptibility to bacterial superinfections. leads to  bacterial debris seen in this [Stanford study] . ,
MicroRNA-9 regulates non-small cell lung cancer cell invasion and migration by targeting eukaryotic translation initiation factor 5A2
Authors: Dawei Zheng
Lebo Sun
Ni Li
Yiming Ni
Guofeng Shao
Huoshun Shi
Qiaoling Pan
Guodong Xu
Minghui Li
Journal: American journal of translational research (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: eIF5A2; invasion and migration; microRNA-9; non-small cell lung cancer (NSCLC).
Affiliations: Department of Cardiothoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou 310006, Zhejiang, China; Department of Cardiothoracic Surgery, The Affiliated Hospital, Ningbo Medical Center Lihuili Hospital, Ningbo UniversityNingbo 315041, Zhejiang, China., Department of Cardiothoracic Surgery, The Affiliated Hospital, Ningbo Medical Center Lihuili Hospital, Ningbo University Ningbo 315041, Zhejiang, China., Department of Respiratory Medicine, Shaoxing People's Hospital, Shaoxing Hospital of Zhejiang University Shaoxing 312000, Zhejiang, China., Department of Cardiothoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University Hangzhou 310006, Zhejiang, China.

Abstract:  MicroRNAs (miRNAs) play a critical role in cancer development and progression. Bioinformatics analyses has identified eukaryotic translation initiation factor 5A2 (eIF5A2) as a target of miR-9. In this study, we attempted to determine whether miR-9 regulates non-small cell lung cancer (NSCLC) cell invasion and migration by targeting eIF5A2 We examined eIF5A2 expression using reverse transcription-quantitative PCR (RT-qPCR) and subsequently transfected A549 and NCI-H1299 NSCLC cells with a miR-9 mimic or miR-9 inhibitor to determine the migration and invasive capability of the cells via wound healing assay and Transwell invasion assay, respectively. E-cadherin and vimentin expression was detected with western blotting. The miR-9 mimic significantly reduced NSCLC cell invasive and metastatic ability, and the miR-9 inhibitor enhanced NSCLC cell migration activity, increasing the number of migrated cells. There was no significant difference between the negative control siRNA and miR-9 mimic groups after knockdown of eIF5A2; western blotting showed that miR-9 regulated E-cadherin and vimentin expression. These data show that miR-9 regulates NSCLC cell invasion and migration through regulating eIF5A2 expression. Taken together, our findings suggest that the mechanism of miR-9-regulated NSCLC cell invasion and migration may be related to epithelial-mesenchymal transition. 

Retracted: No

PubPeer comments:
 Figure 3 caption contains two contradicted sentences. The first sentence is supported by the data presented. ![file] I don t understand how the Targetscan suggested that eIF5A2 is a target gene of miR-9, however, the authors checked whether eIf5A2 regulates miR9! ![file] Unsupported claim. The authors didn t provide any evidence of direct regulation of miR9A and eIF5A2. ![file] ,
Effect of verapamil in the reversal of doxorubicin chemotherapy resistance in advanced gastric cancer
Authors: G-F Fan
B Sun
P-S Fan
X Wang
T-Y Zhang
Y Li
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Gastric carcinoma; chemotherapy resistance; verapamil; P-glycoprotein; glucosylceramide synthase
Affiliations: Cheeloo College of Medicine, Shandong University, Jinan, China. .

Abstract:  Objective: Gastric carcinoma is one of the most common malignant tumors and one of the most common cancer-related fatal diseases. Chemotherapy is considered as the major therapy for advanced gastric cancer, and the curative effect of chemotherapy directly affects the treatment of advanced gastric cancer. Drug resistance of tumor cells is one of the important causes that induces failure of chemotherapy. Previous studies have demonstrated that verapamil (VER) can reverse drug resistance by inhibiting the P-glycoprotein (P-gp), which is one of the main targets of VER. The present study aimed at investigating the function of glucosylceramide synthase (GCS) in the VER-induced reversal of doxorubicin (ADM) chemotherapy resistance in gastric carcinoma. Patients and methods: In the current study, the 4 GC cell line was selected for investigation. The IC50 values of gastric cancer cells were measured using CCK-8 assay. The expression levels of candidate genes in gastric carcinoma cells were measured by RT-qPCR. The expression levels of candidate protein in gastric carcinoma cells were measured by Western blot. The expression of GCS protein in clinical specimens of GC receiving VER+TACE therapy was measured by immunohistochemistry. The test of gastric carcinoma cell apoptosis was measured by Annexin V-FITC/PI double-staining. Results: We found that the expression levels changes of the GCS gene can influence the effects of ADM+VER on cell apoptosis. The role and mechanism of GCS gene in reversing the chemotherapy resistance of gastric carcinoma cells to ADM were explored. Conclusions: In future research, we will explore the mechanism of how GCS affects drug resistance in gastric carcinoma and related signal transduction pathway. 

Retracted: No

PubPeer comments:
 Image duplication in Figure 4: ![file] ,
Involvement of NEAT1/miR-133a axis in promoting cervical cancer progression via targeting SOX4
Authors: Xiaomin Qin
Xianxian Li
Ying Xu
Yun Liu
Xiaogang Mao
Huabing Lv
Li-Yun Yuan
Jinting Zhou
Hui Xing
Min Zhou
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NEAT1; SOX4; cervical cancer; miR-133a.
Affiliations: Department of Obstetrics and Gynecology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China., Department of Nephrology, Huai'an Second People's Hospital and the Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China.

Abstract:  NEAT1 is an important tumor oncogenic gene in various tumors. Nevertheless, its involvement remains poorly studied in cervical cancer. Our study explored the functional mechanism of NEAT1 in cervical cancer. NEAT1 level in several cervical cancer cells was quantified and we found NEAT1 was greatly upregulated in vitro. NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis. For another, microRNA (miR)-133a was downregulated in cervical cancer cells and NEAT1 negatively modulated miR-133a expression. Subsequently, we validated that miR-133a functioned as a potential target of NEAT1. Meanwhile, SOX4 is abnormally expressed in various cancers. SOX4 was able to act as a downstream target of miR-133a and silencing of SOX4 can restrain cervical cancer progression. In addition, in vivo assays were conducted to prove the role of NEAT1/miR-133a/SOX4 axis in cervical cancer. These findings implied that NEAT1 served as a competing endogenous RNA to sponge miR-133a and regulate SOX4 in cervical cancer pathogenesis. To sum up, it was implied that NEAT1/miR-133a/SOX4 axis was involved in cervical cancer development. 

Retracted: No

PubPeer comments:
 Two of the tumors in Figure 7A of this paper look similar to tumors in Figure 7A of Janfei Tu et al. (2018), doi: 10.1002 jcp.27737. Marked with red boxes. ![file] ,
Ligand-bound glutamine binding protein assumes multiple metastable binding sites with different binding affinities
Authors: Jianwei Liu
Lu Zhang
Xilin Jia
Shaowen Wu
Yitao Feng
Zhijun Liu
Dan Wang
Wenning Wang
Journal: Communications Biology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Protein dynamics; Ligand binding; Conformational dynamics; Molecular dynamics simulations; Markov state model (MSM) analysis
Affiliations: State Key Laboratory of Structural Chemistry, Fujian Institute of Research on the Structure of Matter, Chinese Academy of Sciences, Fuzhou, Fujian, China. ., Department of Chemistry, Institutes of Biomedical Sciences, Multiscale Research Institute of Complex Systems, Fudan University, Shanghai, China., State Key Laboratory of Structural Chemistry, Fujian Institute of Research on the Structure of Matter, Chinese Academy of Sciences, Fuzhou, Fujian, China., National Center for Protein Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China., Department of Chemistry, Institutes of Biomedical Sciences, Multiscale Research Institute of Complex Systems, Fudan University, Shanghai, China. .

Abstract:  Protein dynamics plays key roles in ligand binding. However, the microscopic description of conformational dynamics-coupled ligand binding remains a challenge. In this study, we integrate molecular dynamics simulations, Markov state model (MSM) analysis and experimental methods to characterize the conformational dynamics of ligand-bound glutamine binding protein (GlnBP). We show that ligand-bound GlnBP has high conformational flexibility and additional metastable binding sites, presenting a more complex energy landscape than the scenario in the absence of ligand. The diverse conformations of GlnBP demonstrate different binding affinities and entail complex transition kinetics, implicating a concerted ligand binding mechanism. Single molecule fluorescence resonance energy transfer measurements and mutagenesis experiments are performed to validate our MSM-derived structure ensemble as well as the binding mechanism. Collectively, our study provides deeper insights into the protein dynamics-coupled ligand binding, revealing an intricate regulatory network underlying the apparent binding affinity. 

Retracted: No

PubPeer comments:
 The authors cite wrong references to support their claims, thus misleading the reader and attempting to distort published evidence that is in total disagreement with their findings. For example reference 30 in the following sentence, reported the exact opposite of what the authors claim:  ...NMR residual dipolar couplings, and smFRET experiments suggested inter-domain dynamics in ligand-free GlnBP24,30,31,  ,
Ionizing radiation enhances adenoviral vector expressing mda-7/IL-24-mediated apoptosis in human ovarian cancer
Authors: David T Curiel
Zao-Zhong Su
Luni Emdad
Paul B Fisher
Devanand Sarkar
Paul Dent
Irina V Lebedeva
Pankaj Gupta
Parameshwar J Mahasreshti
Journal: Journal of cellular physiology (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Ovarian cancer; mda-7/IL-24; apoptosis; radiosensitization; gene delivery
Affiliations: Department of Urology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, College of Physicians and Surgeons, New York, New York 10032, USA.

Abstract:  Ovarian cancer is the fifth most common cause of cancer-related death in women. Current interventional approaches, including debulking surgery, chemotherapy, and/or radiation have proven minimally effective in preventing the recurrence and/or mortality associated with this malignancy. Subtraction hybridization applied to terminally differentiating human melanoma cells identified melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24), whose unique properties include the ability to selectively induce growth suppression, apoptosis, and radiosensitization in diverse cancer cells, without causing any harmful effects in normal cells. Previously, it has been shown that adenovirus-mediated mda-7/IL-24 therapy (Ad.mda-7) induces apoptosis in ovarian cancer cells, however, the apoptosis induction was relatively low. We now document that apoptosis can be enhanced by treating ovarian cancer cells with ionizing radiation (IR) in combination with Ad.mda-7. Additionally, we demonstrate that mda-7/IL-24 gene delivery, under the control of a minimal promoter region of progression elevated gene-3 (PEG-3), which functions selectively in diverse cancer cells with minimal activity in normal cells, displays a selective radiosensitization effect in ovarian cancer cells. The present studies support the use of IR in combination with mda-7/IL-24 as a means of augmenting the therapeutic benefit of this gene in ovarian cancer, particularly in the context of tumors displaying resistance to radiation therapy. 

Retracted: No

PubPeer comments:
 Figures 3A and 5B. Much more similar than you would expect. https: imgur.com cBGCSIm ,
Upregulation of RHOXF2 and ODF4 Expression in Breast Cancer Tissues
Authors: Maryam Beigom Mobasheri
Mohammad Hossein Modarressi
Lobat Geranpayeh
Golnesa Kazemi-Oula
Soudeh Ghafouri-Fard
Journal: Cell journal (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Breast Cancer; Cancer-Testis Antigen; ODF4; RHOXF2.
Affiliations: Department of Medical Genetics, Tehran University of Medical Sciences, Tehran, Iran ; Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran., Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran., Department of Medical Genetics, Tehran University of Medical Sciences, Tehran, Iran., Department of Surgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Abstract:  Objective: During the past decade, the importance of biomarker discovery has been highlighted in many aspects of cancer research. Biomarkers may have a role in early detection of cancer, prognosis and survival evaluation as well as drug response. Cancer-testis antigens (CTAs) have gained attention as cancer biomarkers because of their expression in a wide variety of tumors and restricted expression in testis. The aim of this study was to find putative biomarkers for breast cancer. Materials and methods: In this applied-descriptive study, the expression of 4 CTAs, namely acrosin binding protein (ACRBP), outer dense fiber 4 (ODF4), Rhox homeobox family member 2 (RHOXF2) and spermatogenesis associated 19 (SPATA19) were ana- lyzed at the transcript level in two breast cancer lines (MCF-7 and MDA-MB-231), 40 invasive ductal carcinoma samples and their adjacent normal tissues as well as 10 fibroadenoma samples by means of quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). Results: All four genes were expressed in both cell lines. Expression of ODF4 and RH- OXF2 was detected in 62.5% and 60% of breast cancer tissues but in 22.5 and 17.5% of normal tissues examined respectively. The expression of both RHOXF2 and ODF4 was upregulated in cancerous tissues compared with their normal adjacent tissues by 3.31 and 2.96-fold respectively. The expression of both genes was correlated with HER2/neu overexpression. RHOXF2 expression but not ODF4 was correlated with higher stages of tumors. However, no significant association was seen between expression patterns and estrogen and progesterone receptors status. Conclusion: ODF4 and RHOXF2 are proposed as putative breast cancer biomarkers at the transcript level. However, their expression at protein level should be evaluated in future studies. 

Retracted: No

PubPeer comments:
 ![file] Figure 3. ,
A novel endosomal sorting complex required for transport (ESCRT) component in Arabidopsis thaliana controls cell expansion and development
Authors: Eugenia Russinova
Marisa S Otegui
Francisca C Reyes
Li Huey Yeun
Hannetz Roschzttardtz
Simone Di Rubbo
Rafael A Buono
Journal: Journal of Biological Chemistry (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cell Biology; Cell Growth; Endosomes; Enzyme Purification; Gene Silencing
Affiliations: From the Department of Botany, University of Wisconsin-Madison, Madison, Wisconsin 53706.

Abstract:  ESCRT proteins mediate membrane remodeling and scission events and are essential for endosomal sorting of plasma membrane proteins for degradation. We have identified a novel, plant-specific ESCRT component called PROS (POSITIVE REGULATOR OF SKD1) in Arabidopsis thaliana. PROS has a strong positive effect on the in vitro ATPase activity of SKD1 (also known as Vacuolar Protein Sorting 4 or VPS4), a critical component required for ESCRT-III disassembly and endosomal vesiculation. PROS interacts with both SKD1 and the SKD1-positive regulator LIP5/VTA1. We have identified a putative MIM domain within PROS that mediate the interaction with the MIT domain of SKD1. Interestingly, whereas MIM domains are commonly found at the C terminus of ESCRT-III subunits, the PROS MIM domain is internal. The heterologous expression of PROS in yeast mutant cells lacking Vta1p partially rescues endosomal sorting defects. PROS is expressed in most tissues and cells types in Arabidopsis thaliana. Silencing of PROS leads to reduced cell expansion and abnormal organ growth. 

Retracted: No

PubPeer comments:
 Possible figure overlap in Figure 2C. Exposure increased 50% in illustration below. *** ![file] , 
 Undated notice on the journal website:  This article is currently under institutional investigation. , 
 https: retractionwatch.com 2016 10 21 cancer-researcher-retracts-19-studies-at-once ,
The effects of MCA-MAO on cAMP pathway in rats with cerebral hemorrhage
Authors: Y-L Niu
Y Jiang
X-F Wang
J-H Xia
Journal: European review for medical and pharmacological sciences (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MCA-MAO; cAMP pathway; cerebral hemorrhage; rats; PKA
Affiliations: Department of Neurology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. .

Abstract:  Objective: To explore the effects of MCA-MAO on the cAMP pathway in rats with cerebral hemorrhage. Materials and methods: Forty SD male rats were randomly divided into four groups: the sham operation group (n=10), the model group (n=10), the negative control group (n=10) and the experimental group (n=10). To prepare rat models for cerebral hemorrhage, autogenous femoral arterial blood was injected into the caudate nucleus. In the case of rats in sham operation group, normal saline was injected into the caudate nucleus. Rats in the negative control group received a proper amount of saline via an injection into the abdominal cavity. Rats in the experimental group were injected with 500 μL/kg MCA-MAO into the abdominal cavity. Five rats from each group were executed after 1 to 3 days, the water contents of gray and white matters were detected using far infrared moisture analyzer, the MAO activity was measured by the histochemical method. The cAMP level was measured by radio-immunity method and the protein kinase A (PKA) level was measured by Western blot. cAMP response element binding (CREB) mRNA expression level was detected by RT-PCR. Results: Water content, MAO activity, cAMP, PKA, and CREB mRNA expression levels in the model, and the negative control groups were significantly higher than those of the sham operation and the experimental groups, the differences were statistically significant (p&lt;0.05). Conclusions: MAO may mediate the pathophysiological process of hemorrhage via cAMP signaling pathway. 

Retracted: No

PubPeer comments:
 A possible concern about Figure 1 was pointed out to me by a reader. * Red boxes: Two panels appear to show an overlap, with an 180 degrees rotation ![file] , 
 I also cannot seem to find any language about animal ethics or approval. Can the authors please shed some light on that? , 
  Glenner staining and MAO activity: **Skin** was cut into 10 u03bcm pieces and incubated in MTT incubation solution at 37 C for 30 to 60 min. Skin?? The images have a grainy appearance, as if copied from an old half-tone reproduction. ,
Casticin potentiates TRAIL-induced apoptosis of gastric cancer cells through endoplasmic reticulum stress
Authors: Jianguo Cao
Fei Liu
Lingzhi Long
Yuan Zhou
Li Tian
Meifang Quan
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Casticin; TRAIL; apoptosis; gastric cancer; death receptors
Affiliations: Medical College, Hunan Normal University, Changsha, China. 

Abstract:  Background: Casticin is one of the main active components obtained from Fructus Viticis and has been reported to exert anti-carcinogenic activity on a variety of cancer cells but the precise mechanism underlying this activity remains unclear. Materials and methods: Apoptotic activities of casticin (1.0 µmol/l) and TRAIL (25, 50 ng/ml) alone or in combination in the gastric cancer cell lines BGC-823, SGC-7901 and MGC-803 were detected by the use of a cell apoptosis ELISA detection kit, flow cytometry (FCM) with propidium iodide (PI) staining and activities of caspase-3, -8 and -9 by ELISA and cleavage of polyADP-ribose polymerase (PARP) protein using western blot analysis. Death receptors (DR) expression levels were evaluated using FCM analysis and western blotting. 2', 7'-dichlorofluorescein diacetate (DCFH-DA) was used as a probe to measure the increase in reactive oxygen species (ROS) levels in cells. Multiple interventions, such as siRNA transfection and pharmacological inhibitors were used to explore the mechanisms of these actions. Results: Subtoxic concentrations of casticin significantly potentiated TRAIL-induced cytotoxicity and apoptosis in BGC-823, SGC-7901 and MGC-803 cells. Casticin dramatically upregulated DR5 receptor expression but had no effects on DR4 or decoy receptors. Deletion of DR5 by siRNA significantly reduced the apoptosis induced by the co-application of TRAIL and casticin. Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production. Casticin downregulated the expression levels of the cell survival proteins cFLIP, Bcl-2, XIAP, and survivin. In addition, casticin also induced the expressions of DR5 protein in other gastric cancer cells (SGC-7901 and MGC-803). Conclusion/significance: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway. 

Retracted: No

PubPeer comments:
 Figure 6A. * Red boxes: In the DR4 panel, lanes 3h and 6h look similar to lanes 12h and 24h. * Green arrows: sharp vertical transitions appear to be visible between certain lanes. Reported to the journal in 2015. ![file] , 
 #1 I agree with the above concerns and also note that there may be a repeated lane in Figure 5B. Could the authors please provide the original uncropped scans? Concerns about images seem to be a recurring issue in papers with at least one common author: https: pubpeer.com search?q=authors%3A Jianguo+Cao *** ![file] ,
Crystal Structures and Anti-Gastric Cancer Activities of Two Cd(II)-Based Coordination Polymers Constructed from Different Donor Ligands
Authors: Zheng, X. -Y.
Yang, P.
Journal: Journal of Structural Chemistry (2020)
Discipline: CHEMISTRY
Keywords: Cd(II); coordination polymers; donor ligands; 2D layered structure; 3D supramolecular structure

Abstract: Two new Cd(II)-containing coordination polymers, namely [Cd(H2O)2(L1)2](NO3)2(1, L1 = 1,3-bis-(imidazol-1-yl)-5-methyl-benzene) and [Cd2(L2)(H2O)6](DMF)3(2, H4L2 = 5,5′-(p-xylylenediamino)-1,1′,3,3′-(benzene-tetra-carboxylic acid), are successfully prepared under the solvothermal conditions using different donor ligands. Complex 1 is a 2D layered structure whose network could be considered as a sql uninodal topological network, while complex 2 reveals a 3D supramolecular structure via H bond interactions between the adjacent 2D layers. Furthermore, the anticancer activity of the two complexes is studied via the CCK-8 assay against the MGC-803 gastric cancer cell lines, which reveals that compound 1 exhibits a significantly stronger activity than compound 2.

Retracted: No

PubPeer comments:
 Could the authors comment on the relevance of Refs [14-15]?  As the most common cell death pathway, the cell apoptosis in MGC-803 gastric cancer cells was assessed by the Annexin V-FITC PI apoptosis kit (BD Biosciences, San Jose, CA, USA) in a flow cytometer according to the protocols [14]. - [14]. D. Zhang, H. Q. Zhang, S. Zhao, Z. G. Li, and S. X. Hou. Int. J. Electrochem. Soc. 2019, 14, 4659. ** Electrochemical Impedance Spectroscopy Evaluation of Corrosion Protection of X65 Carbon Steel by Halloysite Nanotube-Filled Epoxy Composite Coatings in 3.5% NaCl Solution **  After treating with the indicated concentration of compounds 1 and 2, total protein in MGC803 gastric cancer cells was extracted with the total Protein Extraction Kit (Invent Biotechnologies, USA) following the manufactureru2032s protocol [15]. - [15]. S. Guo, R. Chen, H. Li, T. Zhang, and Y. Liu. Int. J. Softw. Eng. Know., 2019, 29, 139. ** Identify Severity Bug Report with Distribution Imbalance by CR-SMOTE and ELM ** , 
  The formation of nanostructures has been further confirmed by scanning electron microscopy (SEM) studies obtained by drop-casting a DMSO-dispersed solution of treated complexes 1 and 2 on a glass surface (Fig. 3). ![file] I think these are TEM images. , 
 Fig 3 again: ![] For comparison, Fig 3 of [Ma et al (2020)] : ![file] UPDATE: Another sighting! Fig 4c of [Cui et al (2020)] , The DLS and the SEM [sic] for the prepared nano 1 and 2 . ![] Fig S5 of [Jiang et al (2020)] ,  The DLS and the SEM *[sic]* image for the treated complexes 1 (a) and 2 : ![file] Fig 2c from [Chen et al (2021)] : ![] Fig 2c from [Liu et al (2020)] : ![] Fig 3 of  Two Cu(II)-coordination polymers: structural diversity and anti-ovarian cancer evaluation ([Yao et al 2021] ).  (c) The DLS and SEM diagrams for complexes 1 and 2 after treatments . ![file] ,
Overexpression of apolipoprotein A1 in the lung abrogates fibrosis in experimental silicosis
Authors: Soo-taek Uh
Hee jeong Kim
Eun suk Koh
Sung-woo Park
An soo Jang
Eun-ju Lee
Choon-sik Park
Eun hee Lee
Yong hoon Kim
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: silica particles; silicosis; inflammation; fibrosis; apolipoprotein A1
Affiliations: Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Gyeonggi-Do, South Korea.

Abstract:  The inhalation of silica particles induces silicosis, an inflammatory and fibrotic lung disease characterized by the early accumulation of macrophages and neutrophils in the airspace and subsequent appearance of silicotic nodules as a result of progressive fibrosis. This study evaluated whether apolipoprotein A1 (ApoA1) protects against ongoing fibrosis and promotes the resolution of established experimental lung silicosis. Crystallized silica was intratracheally administered to 6- to 8-week-old transgenic mice expressing human ApoA1 in their alveolar epithelial cells (day 0). ApoA1 was overexpressed beginning on day 7 (ApoA1_D7 group) or day 15 (ApoA1_D15 group). The mice were sacrificed on day 30 for an evaluation of lung histology; the measurement of collagen, transforming growth factor-b1 and lipoxin A4; and a TUNEL assay for apoptotic cells. The ApoA1_D7 and D15 groups showed significant reductions in the silica-induced increase in inflammatory cells, silicotic nodule area, and collagen deposition compared with the silica-treated ApoA1 non-overexpressing mice. The level of transforming growth factor-b1 decreased in the bronchoalveolar lavage fluid, whereas lipoxin A4 was increased in the ApoA1_D7 and D15 groups compared with the silica-treated ApoA1 non-overexpressing mice. The silica-induced increase in the number of apoptotic cells was significantly reduced in the lungs of mice overexpressing ApoA1. Overexpression of ApoA1 decreased silica-induced lung inflammation and fibrotic nodule formation. The restoration of lipoxin A4 may contribute to the protective effect of ApoA1 overexpression against silica-induced lung fibrosis. 

Retracted: No

PubPeer comments:
 Figure 1D. * Red boxes: The Doxy(-) and Doxy(+) photos appear to show an overlap, albeit rotated differently. ![file] ,
AAV2-VEGF-B gene therapy failed to induce angiogenesis in ischemic porcine myocardium due to inflammatory responses
Authors: Jaakko Lampela
Minttu Turunen
Antti Saraste
Juhani Knuuti
Pekka Poutiainen
Kaisa Valli
Mikko Hakulinen
Niko Järveläinen
Jonna Airaksinen
Satu Siimes
Henna Korpela
Maria Grönman
Jussi Nurro
Tiina Nieminen
Vesa Kärjä
Seppo Ylä-Herttuala
Journal: Gene Therapy (2022)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Therapeutic angiogenesis; gene therapy; coronary artery disease; adeno-associated viruses (AAVs); transduction efficacy
Affiliations: A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland., Turku PET Centre, University of Turku, Turku, Finland., Kuopio University Hospital, Kuopio, Finland., A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland. .

Abstract:  Therapeutic angiogenesis induced by gene therapy is a promising approach to treat patients suffering from severe coronary artery disease. In small experimental animals, adeno-associated viruses (AAVs) have shown good transduction efficacy and long-term transgene expression in heart muscle and other tissues. However, it has been difficult to achieve cardiac-specific angiogenic effects with AAV vectors. We tested the hypothesis whether AAV2 gene transfer (1 × 1013 vg) of vascular endothelial growth factor B (VEGF-B186) together with immunosuppressive corticosteroid treatment can induce long-term cardiac-specific therapeutic effects in the porcine ischemic heart. Gene transfers were delivered percutaneously using direct intramyocardial injections, improving targeting and avoiding direct contact with blood, thus reducing the likelihood of immediate immune reactions. After 1- and 6-month time points, the capillary area was analyzed, myocardial perfusion reserve (MPR) was measured with radiowater positron emission tomography ([15O]H2O-PET), and fluorodeoxyglucose ([18F]FDG) uptake was used to evaluate myocardial viability. Clinical chemistry and immune responses were analyzed using standard methods. After 1- and 6-month follow-up, AAV2-VEGF-B186 gene transfer failed to induce angiogenesis and improve myocardial perfusion and viability. Here, we show that inflammatory responses attenuated the therapeutic effect of AAV2 gene transfer by significantly reducing successful transduction and long-term gene expression despite the efforts to reduce the likelihood of immune reactions and the use of targeted local gene transfer methods. 

Retracted: No

PubPeer comments:
 Figure 2: FDG images at Day -1 and Day 29. Would the authors be able to comment on the similarity between these two images? If these are images of biological structures taken on different days, is such a level of similarity expected? They seem to be almost identical, I ve added a comparison below with the contrast enhanced, and some similarities highlighted with magenta shapes. I assume the blocky shapes in the image are to do with areas sharing the same intensity, but would you expect those to match between images taken on different days? Could the authors comment? ![file] ,
SLC39A7 promotes malignant behaviors in glioma via the TNF-α-mediated NF-κB signaling pathway
Authors: Lian Chen
Zhitao Jing
Long Li
Jinkun Xu
Junshuang Zhao
Jinpeng Zhou
Hao Li
Wei Zheng
Journal: Journal of Cancer (2021)
Discipline: CLINICAL MEDICINE
Keywords: SLC39A7; glioma; invasion; migration.; tumorigenesis.
Affiliations: Department of Neurosurgery, the First Hospital of China Medical University, NO. 155 North Nanjing Street, Shenyang, 110001 China., Department of Histology and Embryology, College of Basic Medical Science, China Medical University, NO. 77 Puhe Road, Shenyang, 110122 China.

Abstract:  Purpose: Several studies have indicated that SLC39A7 plays an important role in tumor progression; however, little is known about the function and mechanism of SLC39A7 in glioma. In this study, we aimed to explore the role of SLC39A7 in glioma development. Patients and methods: Bioinformatic analysis was used to predict the role of SLC39A7 in glioma. Cell viability and Edu assays were used to detect the proliferation of glioma cells. A transwell assay was used to measure the invasion and migration of glioma cells. Western blotting, qPCR and ELISA were used to detect the expression of all molecules. Results: SLC39A7 was found to be highly expressed in high-grade glioma patients with a poor prognosis. Our results indicated that SLC39A7 significantly promoted the proliferation, invasion and migration of glioma cells. Furthermore, SLC39A7 promoted tumorigenesis in orthotopic models. We determined that SLC39A7 promotes the malignant behaviors of glioma by activating the TNF-α-mediated NF-κB signaling pathway. Conclusion: Our study revealed that SLC39A7 promotes the proliferation, invasion and migration of glioma cells via the TNF-α-mediated NF-κB signaling pathway, which provides potential targets for glioma therapy. 

Retracted: No

PubPeer comments:
 Figure 3G and Figure 4G appear to have overlapping images. ![file] , 
 Two images in Figure 7c and in 4e appear to overlap, and one set of images seems to overlap *between* 7c and 4e. *** ![file] ,
Cherry-tree colon: colonoscopic appearance suggesting drug-induced mucosal injury
Authors: David Yates Graham
Gabrio Bassotti
Marco Schiavo-Lena
Maria Pina Dore
Vincenzo Villanacci
Alessandra Manca
Giuseppe Sabatino
Sara Soro
Journal: Internal and emergency medicine (2014)
Discipline: CLINICAL MEDICINE
Keywords: Drug-induced damage; gastrointestinal mucosa; lower gut; colon; colonoscopic findings
Affiliations: Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy.

Abstract:  Drug-induced damage to the gastrointestinal mucosa has been mainly focused on damage in the upper tract. However, increasing evidence suggests that commonly used drugs may also affect the mucosa of the lower gut, and particularly in the colon. The aim of this study was to report that fairly homogeneous colonoscopic findings, correlate with histological evidence of drug-induced mucosal injury. Charts of patients with the "cherry tree" colonoscopic aspect were reviewed to correlate the endoscopic and histological findings for a possible association with the use of drugs. Data from 29 patients (5 men, 24 women, age range 16-76 years) with the "cherry tree" colonoscopic findings were analyzed. Histology revealed an increase in eosinophils in the left colon in 23 patients, pseudomelanosis coli in 3, and microscopic colitis in 3. The findings were associated with proton pump inhibitors in 19 (65.5 %), non-steroidal anti-inflammatory drugs or statins (3 cases each), and other drugs [4 cases, including estroprogestinics (1), antidepressants (2), and thyroxin (1)]. The "cherry tree" colonoscopic appearance suggests drug-induced colonic damage. Awareness of this association may prevent unnecessary, expensive and time-consuming procedures. 

Retracted: No

PubPeer comments:
 This paper was published in 2014 but refers to patients observed from 2004-07. Patients and methods Data from patients undergoing colonoscopy in the period from January 2004 to January 2007, with characteristic endoscopic features (see below), and in whom histology was available from multiple colonic segments (involved and non-involved areas) were analyzed. More specifically, all drugs taken by the patients for at least 2 weeks in the 2 months before colonoscopy were thoroughly checked in the endoscopic chart and, when necessary, by phone interview. The Methods does not explain where the study was carried out. Will the authors provide such details (which are deemed essential by guidelines in reporting clinical studies)? Could also explain image duplications from 2009? ![file] ![file] , 
 The same image has been re-used to illustrate different clinical settings. Could the authors explain? ![file] , 
 ![file] ,
Treatment Activity of a New Pr(III) Coordination Polymer on Diabetic Retinopathy by Regulating miR-107/HMGB1 in Retinal Vascular Cells
Authors: Yu, Fei-Fei
Du, Yun-Hong
Pang, Guo-Long
Journal: Journal of Cluster Science (2021)
Discipline: CHEMISTRY
Keywords: lanthanide coordination polymer; miR-107; diabetic retinopathy; retinal vascular cells; inflammation

Abstract: A lanthanide coordination polymer (Ln-CP), {Pr2(PBA)3(H2O)3]·DMF·3H2O}n (1), was synthesized using 5-(4-pyridin-3-yl-benzoylamino)-isophthalic acid (H2PBA), a tripodal carboxylic ligand. Moreover, the relative expression of miR-107 was evaluated through RT-PCR. miR-107 effect was then detected with the CCK-8 assay. ROS detection and ELISA were used to assess the inflammatory response in retinal vascular cells. miR-107 downstream regulation was also investigated. TargetScan was applied to predict the latent proteins that bind to miR-107 via the 3′-UTR, which was demonstrated in-depth through luciferase activity assay. All outcomes indicated that the miR-107 level was lower in retinal vascular cells in a diabetic retinopathy (DR) model. miR-107 expression could further regulate the proliferation of retinal vascular cells and inhibit inflammation, thereby playing a protective role in the function of retinal vascular cells. Thus, miR-107 may be an upstream regulatory factor of high-mobility group box 1, and let 7-5p may be a latent molecular target to treat DR.

Retracted: No

PubPeer comments:
  This **preformation** was conducted in accordance with the protocol of the manufacturer with some modification [23]. In a typical procedure, RNA was isolated from retinal vascular cells of DR patients or ARPE-19 cells after transfection by using TRIzol Reagent...  In a typical procedure, in the logarithmic-growth phase, ARPE-19 was harvested and inoculated on 96-well plates at 1 u00d7 10 4 cells well **ultimate destiny** and subsequently transfected... These choices of words are curious. They are also common in [the products of a coordination-polymer papermill] . ![] ,
Stat3 activation of NF-{kappa}B p100 processing involves CBP/p300-mediated acetylation
Authors: Nagalakshmi Nadiminty
Xin Lin
Allen C Gao
Donald L Trump
Soo Ok Lee
Wei Lou
Journal: Proceedings of the National Academy of Sciences of the United States of America (2006)
Discipline: Multidisciplinary
Keywords: noncanonical NF-kappaB signaling pathway; p100; p52; Stat3; IKKalpha
Affiliations: Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

Abstract:  Activation of the noncanonical NF-kappaB signaling pathway involved in the proteolytic processing of NF-kappaB p100 to p52 is tightly regulated, and overproduction of p52 leads to lymphocyte hyperplasia and transformation. We have demonstrated that active but not latent Stat3, expressed in many types of human cancers involved in cell proliferation and survival, induces p100 processing to p52 by activation of IKKalpha and subsequent phosphorylation of p100. The Stat3-mediated p100 processing to p52 requires activation of Stat3 by the acetyltransferase activity of cAMP-response element-binding protein (CREB)-binding protein (CBP)/p300. A mutant of Stat3 defective in acetylation blocked Stat3-mediated p100 processing to p52 and acted as a dominant negative in blocking the production of p52. Furthermore, overexpression of p52 protected cells from apoptotic cell death. Thus, activation of the processing of p100 to p52 by Stat3 may represent one of the common pathways used by cancer cells to survive and escape therapy. 

Retracted: No

PubPeer comments:
 This review paper appears to be unexpectedly similar to a 2015 PhD thesis by Alexander Blum at Arizona State University called  Evaluating Applications of a Telemedicine Taxonomy on the Classification of Research . That 20135 thesis can be found here: https: core.ac.uk download pdf 79576463.pdf Of note, several other review papers by Zhang and Zhang published in Oncology Letters from the same publisher, Spandidos, have been retracted for plagiarism of other PhD theses. See DOIs 10.3892 ol.2016.5093, 10.3892 ol.2016.5107, 10.3892 ol.2016.5134, 10.3892 ol.2016.5200, 10.3892 ol.2016.5242, 10.3892 ol.2016.5260, 10.3892 ol.2016.5302, and 10.3892 ol.2016.5322. Here is a marked-up version of the text by Zhang and Zhang 2016, with highlighted text showing similarities to the thesis. Generated in SimTexter . On the left is the original 2015 text by Blum, on the right the Zhang and Zhang 2016 review. ![file] Two close-up views in higher resolution: ![file] ![file] ,