PReD-Bench/PRed-Bench huggingface dataset:
Expression of serum microRNA-378 and its clinical significance in laryngeal squamous cell carcinoma
Authors: D Yang
G Zhang
H-F Zhou
Y Xu
Y-P Lin
Journal: European review for medical and pharmacological sciences (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miRNA-378; laryngeal squamous cell carcinoma; serum; expression; clinical significance
Affiliations: Department of Otorhinolaryngology, Department of Neurosurgery; Tianjin Medical University General Hospital, Tianjin, China. .

Abstract:  Objective: Studies have demonstrated that miRNA -378 expressed in various malignant tumors. In the present study, we aim to explore the expression of serum miRNA-378 and its clinical significance in laryngeal squamous cell carcinoma (LSCC) patients. Patients and methods: A total of 127 LSCC patients, 127 vocal cord polyp (VCP) and 130 healthy controls were selected. Results: The miRNA-378 level in LSCC and VCP group was significantly higher compared to healthy control, and LSCC group has the highest miRNA-378 level. The miRNA-378 level was both decreased significantly in LSCC and VCP group when compared with the same group after surgery. When compared with healthy control, VCP group has a higher miRNA-378 level but has no statistical difference (p&gt;0.05) while LSCC group has a statistical difference (p&lt;0.05) higher miRNA-378 compare with healthy control. The miRNA-378 expression is correlated with clinical stage and differentiation degree, but did not correlate with patient's age, gender distribution, operation mode, and tumor diameter. The AUC of miRNA-378 was 0.888, 95% confidence interval was 0.849 to 0.929, and AUC hypothesis testing was statistically significant (p&lt;0.001). Conclusions: miRNA-378 could be used in the diagnosis and the prediction of the postoperative curative effect of laryngeal cancer (LSCC). 

Retracted: No

PubPeer comments:
 Figure 2C appears to have two images with a common source. *** ![file] ,
miR-126 Suppresses Invasion and Migration of Malignant Glioma by Targeting Mature T Cell Proliferation 1 (MTCP1)
Authors: Huaqiang Liu
Jinfeng Wu
Liangbo Han
Jinkai Liu
Journal: Medical Science Monitor (2018)
Discipline: CLINICAL MEDICINE
Keywords: miR-126; malignant glioma; progression; treatment; expression
Affiliations: Department of Neurosurgery, Weifang Yidu Central Hospital, Weifang, Shandong, China (mainland)., Department of Radiotherapy, Weifang Yidu Central Hospital, Weifang, Shandong, China (mainland)., Department of Neurosurgery, Weifang People's Hospital, Weifang, Shandong, China (mainland).

Abstract:  BACKGROUND The aim of this study was to assess the utility of miR-126 in promoting malignant glioma progression and determine if miR-126 might be a target for malignant glioma treatment. MATERIAL AND METHODS The expression of miR-126 in malignant glioma tissues and cells was detected by reverse transcription polymerase chain reaction (RT-PCR). Western blot analysis was used to detect changes in protein levels. Transwell assay was applied to assess the migration and invasion in vitro. Luciferase reporter assay was used to confirm the binding of miR-126 and mature T cell proliferation 1 (MTCP1). A nude mouse tumor model was used to assess the molecular mechanism in vivo. RESULTS The expression level of miR-126 in patients with stage III~IV malignant glioma was significant lower than that in patients with stage I~II. In different malignant glioma cell lines, the expression was significantly reduced in U87MG. Compared with the control mimics group, the expression of MTCP1 was significantly decreased. The results of Transwell assay showed that the invasiveness and migration in the miR-126 mimics group was significantly lower than in the control mimics groups. miR-126 mimics did not affect luciferase activity in the Mut-miR-126/MTCP1 group, while miR-126 mimics reduced luciferase activity by 54% in the Wt-miR-126/MTCP1 group. The results of invasion showed that the invasion ability in the miR-126 inhibitor group was significantly increased compared with that in the normal control (NC) group, while the invasion and migration abilities in the MTCP1 siRNA group were significantly increased. After 6 weeks, the tumor volume in the miR-126 inhibitor group was significantly increased, while that in the MTCP1 siRNA group was significantly decreased. CONCLUSIONS miR-126 inhibits the migration of malignant glioma cells by inhibiting MTCP1. 

Retracted: No

PubPeer comments:
 Figs 3 and 5.  miR-126 inhibited the migration and invasion of U87MG (u00d7400). (A) Transwell method was used to detect the invasion of U87MG. (B) Transwell method was used to detect the migration of U87MG ...  (A, B) The expression of MTCP1 affected the migration and invasion of U87MG (u00d7400) . ![file] Could the authors clarify whether the marked panel are migrating or invading cells that were transfected with irrelevant control mimics, or not manipulated at all (NCs)? ,
Amplification and overexpression of CTTN (EMS1) contribute to the metastasis of esophageal squamous cell carcinoma by promoting cell migration and anoikis resistance
Authors: Yu Zhang
Yun-Tian Sun
Ming-Rong Wang
Man-Li Luo
Yan Cai
Qi-Min Zhan
Xin Xu
Xun Zhang
Min Wu
Xiao-Ming Shen
Fang Wei
Journal: Cancer Research (2006)
Discipline: CLINICAL MEDICINE
Keywords: Chromosome 11q13; Esophageal squamous cell carcinoma; Cortactin gene; CTTN; Lymph node metastasis
Affiliations: State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

Abstract:  Gain of chromosome 11q13 is a common event in esophageal squamous cell carcinoma (ESCC). The cortactin gene (CTTN, also EMS1), located at 11q13, plays a pivotal role in coupling membrane dynamics to cortical actin assembly. This gene has been implicated in the motility of several types of cells. In the present study, we found that the amplification and overexpression of the CTTN gene was associated with lymph node metastasis in ESCC. Functional analysis by small interfering RNA-mediated silencing of CTTN revealed that in addition to the effect on cell migration, CTTN influenced cell invasiveness by anoikis resistance. In vivo assay showed that inhibition of CTTN expression also decreased tumor growth and lung metastasis of ESCC cells. At the molecular level, we showed for the first time that the protective role of CTTN in anoikis resistance was correlated with the activation of the phosphatidylinositol 3-kinase/Akt pathway. Overall, the data suggest that CTTN is an oncogene in the 11q13 amplicon and exerts functions on tumor metastasis in ESCC. 

Retracted: No

PubPeer comments:
 The cell line used in this paper is a HeLa-contaminated cell line. , 
 Figure 2B continued. Much more similar than expected. https: imgur.com Rti1lbx ![file] ,
LincRNA-ROR is activated by H3K27 acetylation and induces EMT in retinoblastoma by acting as a sponge of miR-32 to activate the Notch signaling pathway
Authors: Yali Gao
Jun Zhang
Xiaoling Luo
Journal: Cancer Gene Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: lincRNA-ROR; retinoblastoma; metastasis; miR-32-5p; Notch signaling pathway
Affiliations: Department of Ophthalmology, The Second Clinical Medical College (Shenzhen People's Hospital), Jinan University, Shenzhen, China., Department of Obstetrics and Gynecology, The Second Clinical Medical College (Shenzhen People's Hospital), Jinan University, Shenzhen, China. .

Abstract:  Recent studies have suggested that lincRNA-ROR is involved in the tumorigenesis of different types of cancers. However, the role of lincRNA-ROR in retinoblastoma has not been determined. We investigated lincRNA-ROR levels in 58 retinoblastoma and adjacent non-tumor tissues by quantitative reverse transcription PCR. Recurrence-free survival was analyzed using Cox regression analyses. Cell migration and invasion abilities were detected by wound-healing, Transwell invasion, and bioluminescence imaging assays. Western blotting was performed to detect epithelial-mesenchymal transition markers. Interactions between lincRNA-ROR, miR-32-5p, and Notch1 were confirmed by Luciferase, RNA pull-down, and RIP assays. Histone acetylation was detected by chromatin immunoprecipitation assays. We showed that lincRNA-ROR was significantly upregulated in retinoblastoma tissues, and overexpression of lincRNA-ROR was significantly correlated with optic nerve invasion, nodal or distant metastasis, and recurrence. We also showed that lincRNA-ROR is a critical promoter of retinoblastoma cell metastasis, both in vivo and in vitro. Further, we demonstrated that lincRNA-ROR activates the Notch signaling pathway by acting as a sponge of miR-32-5p. Upregulation of lincRNA-ROR was attributed to the CBP-mediated H3K27 acetylation at the promoter region. Our results reveal a potential competing endogenous RNA regulatory pathway, in which lincRNA-ROR modulates the epithelial-mesenchymal transition program by competitively binding to endogenous miR-32-5p and regulating Notch signaling pathway activity in retinoblastoma cells, which may provide new insights into novel molecular therapeutic targets for retinoblastoma. 

Retracted: No

PubPeer comments:
 Figure 6B contains a duplicated (and rotated) element with slightly altered color: ![file] ,
An alternatively spliced survivin variant is positively regulated by p53 and sensitizes leukemia cells to chemotherapy
Authors: Ningxi Zhu
Lubing Gu
Fengzhi Li
Muxiang Zhou
Harry W Findley
Journal: Oncogene (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Survivin; p53; apoptosis; variants; leukemia
Affiliations: Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322, USA.

Abstract:  Survivin is a unique member of the inhibitor of apoptosis protein family, and its expression is regulated by p53. Recent identification of several functionally divergent survivin variants augments the complexity of survivin action as well as its regulation. Here we report that survivin-2B (retaining a part of intron 2 as a cryptic exon) is positively regulated by p53, and its overexpression plays a role in sensitizing leukemia cells to chemotherapeutic drug doxorubicin. Doxorubicin treatment activated p53, downregulated survivin and survivin-DeltaEx3 but upregulated survivin-2B in EU-3, an acute lymphocytic leukemia (ALL) cell line with wild-type (wt)-p53 phenotype. In contrast, doxorubicin treatment failed to induce these alterations in EU-6 cells, a mutant-p53 ALL cell line. To specify the role of wt-p53 in regulating survivin and its variants, a temperature-sensitive p53 mutant plasmid p53-143 was transfected into EU-4, a p53-null ALL cell line, to establish a subline EU-4/p53-143. When EU-4/p53-143 cell culture was shifted from 37.5 degrees C to the wt-p53-permissive temperature (32.5 degrees C), the expression of survivin and survivin-DeltaEx3 was decreased whereas survivin-2B expression was increased, confirming the distinct regulatory effect of p53 on survivin and its variants. To clarify the role of survivin-2B in the process of apoptosis, survivin-2B cDNA was cloned into pcDNA3HA vector and transfected into EU-4 cells. Enforced expression of survivin-2B in EU-4 cells inhibited cell growth and sensitized these cells to doxorubicin-induced apoptosis. These results suggest that survivin-2B variant is a proapoptotic factor and its expression is upregulated by p53. 

Retracted: No

PubPeer comments:
 Figure 2c. Much more similar than you would expect. https: imgur.com acsLj2J ,
Interplay between c-Src and the APC/C co-activator Cdh1 regulates mammary tumorigenesis
Authors: Shulong Jiang
Pier Paolo Pandolfi
Amer A Beg
Mengyu Xie
Qing Yin
Margaret R Little
Lixin Wan
Su Jung Song
Xiu Yin
Tao Han
Ming Chen
Hong Zheng
Journal: Nature Communications (2019)
Discipline: Multidisciplinary
Keywords: Anaphase Promoting Complex (APC); Cdh1; c-Src; tumorigenesis; cancer progression
Affiliations: Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA., Department of Oncology, Affiliated Jining NO.1 People's Hospital of Jining Medical University, Jining, Shandong, 272000, P.R. China., Department of Oncology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, P.R. China., Department of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA., Department of Cancer Biology PhD Program, University of South Florida, Tampa, FL, 33620, USA., Nova Southeastern University, Fort Lauderdale, FL, 33314, USA., Cancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA., Department of Pathology, Duke University School of Medicine, Duke Cancer Institute, Duke University, Durham, NC, 27710, USA., Soonchunhyang Institute of Medi-bio Science, Soonchunhyang University, Cheonan-si, Chungcheongnam-do, 31151, Republic of Korea., Department of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA., Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA. ., Department of Cutaneous Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA. .

Abstract:  The Anaphase Promoting Complex (APC) coactivator Cdh1 drives proper cell cycle progression and is implicated in the suppression of tumorigenesis. However, it remains elusive how Cdh1 restrains cancer progression and how tumor cells escape the inhibition of Cdh1. Here we report that Cdh1 suppresses the kinase activity of c-Src in an APC-independent manner. Depleting Cdh1 accelerates breast cancer cell proliferation and cooperates with PTEN loss to promote breast tumor progression in mice. Hyperactive c-Src, on the other hand, reciprocally inhibits the ubiquitin E3 ligase activity of APCCdh1 through direct phosphorylation of Cdh1 at its N-terminus, which disrupts the interaction between Cdh1 and the APC core complex. Furthermore, pharmacological inhibition of c-Src restores APCCdh1 tumor suppressor function to repress a panel of APCCdh1 oncogenic substrates. Our findings reveal a reciprocal feedback circuit of Cdh1 and c-Src in the crosstalk between the cell cycle machinery and the c-Src signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 5C appears to have a repeated image. *** ![file] ,
RETRACTED: Three-Minutes Sitting Test for evaluating lumbar foraminal stenosis: A preliminary report
Authors: Tetsutaro Mizuno
Yuichi Kasai
Toshihiko Sakakibara
Journal: Journal of Spinal Cord Medicine (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Retracted; Article; Research; Paper;
Affiliations: Department of Spinal Surgery and Medical Engineering, Mie University Graduate School of Medicine, Tsu City, Japan

Abstract:  This article has been retracted. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: www.tandfonline.com doi full 10.1080 10790268.2018.1473673 We, the Editor and Publisher of The Journal of Spinal Cord Medicine, have retracted the following article which was published online on 11 January 2018: Tetsutaro Mizuno, Toshihiko Sakakibara Yuichi Kasai, u201cThree-Minutes Sitting Test for evaluating lumbar foraminal stenosis: A preliminary reportu201d DOI: 10.1080 10790268.2017.1420537. The Journal of Spinal Cord Medicine. The authors of this article have asked that their report be retracted after being notified by their Institutional Review Board that the method of acquiring patient consent is not adequate in this study. Patient consent was obtained after the survey in this report had been completed, rather than prior to the survey being administered. We have been informed in our decision-making by our policy on publishing ethics and integrity and the guidance of COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u2018Retractedu2019. ,
Mitochondria-mediated disturbance of fatty acid metabolism in proximal tubule epithelial cells leads to renal interstitial fibrosis
Authors: Q He
Y-W Li
X-X Jiang
W Shen
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Mitochondria; Fatty acid metabolism; Renal interstitial fibrosis; Tubulointerstitial; Dysfunction
Affiliations: Department of Nephrology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China. .

Abstract:  Objective: To investigate the role of mitochondria-mediated fatty acid metabolism in proximal tubule cells in renal interstitial fibrosis. Materials and methods: Intraperitoneal injection of folate was performed to induce renal interstitial fibrosis in mice. Polymerase chain reaction (PCR) was used to detect the expression of cytochrome c oxidase subunit IV (COX4IL) and phosphoenolpyruvate carboxykinase 1 (PCK1) in samples. Electron microscope was used to detect the activity of mitochondria. Serum creatinine and urea nitrogen were chosen as evaluation criteria for renal function. Western-blotting was used to detect protein expression of cells. Immunohistochemistry was used to test renal structure and deposition of collagen. Results: In renal interstitial fibrosis, mitochondria mediated the dysfunction and the promotion of tubulointerstitial fatty acid metabolism. Besides, it could also reduce renal interstitial fibrosis and alleviate the fatty acid metabolism of tubulointerstitial fibrosis. Conclusions: Mitochondrial dysfunction induced fatty acid metabolism is an important factor to promote the progress of renal interstitial fibrosis. Intervention of related targets of fatty acid metabolism is expected to become a new treatment for renal interstitial fibrosis. 

Retracted: Yes

PubPeer comments:
 This February 2018 article has been withdrawn in November 2018. The retraction notice can be found here, but gives no further insight as to what has happened. https: www.europeanreview.org article 16240 ,
IL-10 supplementation increases Tregs and decreases hypertension in the RUPP rat model of preeclampsia
Authors: Ralf Dechend
Gerd Wallukat
Lorena Amaral
Janae Moseley
Florian Herse
Jessica Faulkner
Tarek Ibrahim
Denise Cornelius
Babbette LaMarca
Adrienne Paige
Ashlyn Harmon
Journal: Hypertension in pregnancy (2015)
Discipline: CLINICAL MEDICINE
Keywords: Hypertension; inflammation; pregnancy..
Affiliations: Pharmacology, University of Mississippi Medical Center , Jackson, MS , USA .

Abstract:  Objective: The reduced uterine perfusion pressure (RUPP) rat model of preeclampsia was used to determine the effects of added interleukin-10 (IL-10) on Tregs and hypertension in response to placental ischemia and how the decrease in these anti-inflammatory factors mediates the pathophysiology of preeclampsia. Methods: IL-10 (2.5 ng/kg/d) was infused via osmotic mini-pump implanted intraperitoneally on day 14 of gestation and, at the same time, the RUPP procedure was performed. Results: IL-10 reduced mean arterial pressure (p &lt; 0.001), decreased CD4(+) T cells (p = 0.044), while increasing Tregs (p = 0.043) which led to lower IL-6 and TNF-α (p = 0.008 and p = 0.003), reduced AT1-AA production (p &lt; 0.001), and decreased oxidative stress (p = 0.029) in RUPP rats. Conclusion: These data indicate that IL-10 supplementation increases Tregs and helps to balance the altered immune system seen during preeclampsia. 

Retracted: No

PubPeer comments:
 Hello, In figure 2 C I dont understand why the gating SS and FS for Lymphocyte is differente for the one that has IL-10 and the ones that don t. Did you explain it somewhere? All the best, , 
 I m confused about this too. It looks like the gates were arbitrarily changed. ,
Contribution of adipose triglyceride lipase and hormone-sensitive lipase to lipolysis in hMADS adipocytes
Authors: Amandine Girousse
Johan Jocken
Gérard Ailhaud
Anne-Marie Rodriguez
Véronic Bezaire
Britta M Stenson
Aline Mairal
Dominique Langin
Peter Arner
Mikael Ryden
Carole Ribet
Rodica Anesia
Christian Dani
Jurga Laurencikiene
Corinne Lefort
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Lipolysis; Triglycerides; Adipose triglyceride lipase (ATGL); Hormone-sensitive lipase (HSL); CGI-58
Affiliations: INSERM U858, Laboratoire de Recherches sur les Obésités, F-31432 Toulouse, France.

Abstract:  Lipolysis is the catabolic pathway by which triglycerides are hydrolyzed into fatty acids. Adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) have the capacity to hydrolyze in vitro the first ester bond of triglycerides, but their respective contributions to whole cell lipolysis in human adipocytes is unclear. Here, we have investigated the roles of HSL, ATGL, and its coactivator CGI-58 in basal and forskolin-stimulated lipolysis in a human white adipocyte model, the hMADS cells. The hMADS adipocytes express the various components of fatty acid metabolism and show lipolytic capacity similar to primary cultured adipocytes. We show that lipolysis and fatty acid esterification are tightly coupled except in conditions of stimulated lipolysis. Immunocytochemistry experiments revealed that acute forskolin treatment promotes HSL translocation from the cytosol to small lipid droplets and redistribution of ATGL from the cytosol and large lipid droplets to small lipid droplets, resulting in enriched colocalization of the two lipases. HSL or ATGL overexpression resulted in increased triglyceride-specific hydrolase capacity, but only ATGL overexpression increased whole cell lipolysis. HSL silencing had no effect on basal lipolysis and only partially reduced forskolin-stimulated lipolysis. Conversely, silencing of ATGL or CGI-58 significantly reduced basal lipolysis and essentially abolished forskolin-stimulated lipolysis. Altogether, these results suggest that ATGL/CGI-58 acts independently of HSL and precedes its action in the sequential hydrolysis of triglycerides in human hMADS adipocytes. 

Retracted: No

PubPeer comments:
 In Figure 6c, the curves for the PI in untreated cells (gray) are identical for the two different cell types. ![file] , 
 Dear Indigofera, Please note that shaded curves in the aforesaid histograms represent unstained FACS control and should not be confused with untreated wild-type or MyD88 knockout DCs. Untreated wild-type and MyD88 knockout DCs are denoted by unshaded curves in upper and lower left histograms, respectively. ,
Stat3 inhibitor Stattic exhibits potent antitumor activity and induces chemo- and radio-sensitivity in nasopharyngeal carcinoma
Authors: Francois X Claret
Yunbao Pan
Fuling Zhou
Ronghua Zhang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Nasopharyngeal carcinoma; Stat3; Stattic; Chemoradiotherapy; Resistance
Affiliations: Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Abstract:  Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus-associated malignancy most common in East Asia, Africa and Alaska. Radiotherapy and cisplatin-based chemotherapy are the main treatment options. Unfortunately, disease response to concurrent chemoradiotherapy varies among patients with NPC, and many cases are resistant to cisplatin and radiotherapy. Signal transducer and activator of transcription 3 (Stat3) has been implicated in the development and progression of various solid tumors. In this study, we assessed the activation and expression of Stat3 in NPC cells. We found that Stat3 was activated and could be blocked by the small molecule inhibitor Stattic. The inhibition of Stat3 in NPC cells by Stattic decreased the expression of cyclin D1 in a dose- and time-dependent manner. Thus, Stattic was used to target Stat3 in NPC cell lines. We found that Stattic could inhibit cell viability and proliferation in NPC cells and significantly induced apoptosis. Additionally, Stat3 transfection attenuated, whereas Stat3 knockdown enhanced, the effects of Stattic upon cell viability inhibition and apoptosis induction. Furthermore, Stattic sensitized NPC cells to cisplatin and ionizing radiation (IR) by preventing cell proliferation and inducing apoptosis. Taken together, Stattic inhibit Stat3 and display antitumor effect in NPC, and enhanced chemosensitivity and radiosensitivity in NPC. Therefore, our findings provide the base for more rational approaches to treat NPC in the clinic. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
RETRACTED: Co-fermentation of magnesium oxide-treated corn stover and corn stover liquor for cellulosic ethanol production and techno-economic analysis
Authors: Meng Zhang
Donghai Wang
Haibo Huang
Jun Li
Journal: Bioresource Technology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Co-fermentation; Corn stover; Escherichia coli KO11; MgO pretreatment; Techno-economic analysis.
Affiliations: Department of Biological and Agricultural Engineering, Kansas State University, Manhattan, KS 66506, United States., Department of Food Science and Technology, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, United States. Electronic address: ., Department of Industrial and Manufacturing Systems Engineering, Kansas State University, Manhattan, KS 66506, United States., Department of Biological and Agricultural Engineering, Kansas State University, Manhattan, KS 66506, United States. Electronic address: .

Abstract:  MgO is an effective catalyst to reduce the recalcitrant structure of corn stover and reduce sugar degradation during pretreatment. To evaluate the economic feasibility of MgO pretreatment, techno-economic analysis was performed at a commercial scale of 700,000 MT stover per year based on the collected experimental data. Compared to LHW pretreatment, MgO pretreatment reduced total capital investment due to elimination of solids washing and increased ethanol yield by 78.4 L/MT stover due to higher xylose yield (53.4 vs 10.9%), thus resulted in a lower minimum ethanol selling price (MESP) of $0.72/liter. Although washing of MgO-pretreated solids improved glucose (73.0 vs 69.5%) and xylose (66.0 vs 53.4%) yields, MESP did not decrease but increase by $0.08/liter due to the high capital cost of solid-liquid separation unit. Tween 80 also improved glucose (73.1 vs 69.5%) and xylose (62.6 vs 53.5%) yields. However, its high cost limited its economic feasibility in ethanol production. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: www.sciencedirect.com science article pii S0960852420300894 This article has been retracted at the request of the Authors and the Editor-in-Chief. This article contains some flaws in experimental method protocol used. The major issue is that the filtration aperture (cheese cloth) used for solid and liquid separation after biomass pretreatment was not well controlled over the research period. Using used-cheese-cloths with varied aperture size unintentionally caused a large variation in mass recovery and chemical composition of treated biomass. New cheese cloth should be used each time to assure reproducibility. ,
LncRNA LINC01116 competes with miR-145 for the regulation of ESR1 expression in breast cancer
Authors: S-Q Ding
Q Chen
H-B Hu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; LINC01116; breast cancer; Gene Expression Omnibus; GSE54002
Affiliations: Department of General Surgery, Shenzhen Guangming New District Central Hospital, Shenzhen, China. .

Abstract:  Objective: To investigate the biological role and clinical significance of long non-coding RNAs (lncRNA) LINC01116 in breast cancer. Materials and methods: In the public database Gene Expression Omnibus (GEO), the breast cancer data set GSE54002 was screened for differentially expressed lncRNA LINC01116 in breast cancer tissues and paracancerous tissues. Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of LINC01116 in 64 breast cancer tissues and 30 normal breast tissues. Level of LINC01116 and clinicopathological parameters of breast cancer were statistically analyzed. The effect of LINC01116 in breast cancer cells was investigated after knockdown of LINC01116. Luciferase reporter gene was further used to investigate the mechanism of endogenous RNA (ceRNA). Results: Results of GSE54002 showed that the expression of LINC01116 in breast cancer tissues was significantly increased. In clinical samples, the level of LINC01116 in patients with breast cancer was significantly increased, which was correlated with the overall survival, tumor size and tumor node metastasis (TNM) stage in patients, but not correlated with the age, sex and lymph node metastasis (p&gt;0.05). LINC01116 can act as an endogenous sponge and bind directly to miR-145, resulting in the up-regulation of estrogen receptor 1 (ESR1), a target gene of miR-145. Conclusions: LncRNA LINC01116 is highly expressed in breast cancer and is a new prognostic biomarker in breast cancer. Our study establishes a new link between LINC01116, miR-145 and ESR1. 

Retracted: No

PubPeer comments:
null, 
null, 
 https: www.straitstimes.com singapore 3-spore-based-scientists-linked-to-research-fraud ,
CX3CR1 deficiency suppresses activation and neurotoxicity of microglia/macrophage in experimental ischemic stroke
Authors: Jiong Shi
Fu-Dong Shi
Jun-Xiang Yin
Yan Gan
Zhiwei Tang
Qiang Liu
Qingwei Liu
Journal: Journal of Neuroinflammation (2014)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Chemokine; CX3CR1; microglia; macrophage; ischemic brain injury
Affiliations: Department of Neurology and the BNI-ASU Center for Preclinical Imaging, Barrow Neurological Institute, St, Joseph's Hospital and Medical Center, 350 West Thomas Road, Phoenix, Arizona 85013, USA. .

Abstract:  Background: Chemokine (C-X3-C motif) ligand 1 (CX3CL1)/ CX3C chemokine receptor 1 (CX3CR1) signaling is important in modulating the communication between neurons and resident microglia/migrated macrophages in the central nervous system (CNS). Although CX3CR1 deficiency is associated with an improved outcome following ischemic brain injury, the mechanism of this observation is largely unknown. The aim of this study was to investigate how CX3CR1 deficiency influences microglia/macrophage functions in the context of its protection following brain ischemia. Methods: Wild-type (WT) and CX3CR1-deficient (CX3CR1⁻/⁻) mice were subjected to transient middle cerebral artery occlusion (MCAO) and reperfusion. The ischemic brain damage was monitored by rodent high-field magnetic resonance imaging. Neurological deficit was assessed daily. Neuronal apoptotic death and reactive oxygen species (ROS) production were analyzed by immunostaining and live imaging. Activation/inflammatory response of microglia/macrophage were assessed using immunohistochemistry, flow cytometry, 5-bromo-2-deoxyuridine labeling, cytokine ELISA, and real-time PCR. Results: CX3CR1⁻/⁻ mice displayed significantly smaller infarcts and less severe neurological deficits compared to WT controls, following MCAO. In addition, CX3CR1⁻/⁻ MCAO mice displayed fewer apoptotic neurons and reduced ROS levels. Impaired CX3CR1 signaling abrogated the recruitment of monocyte-derived macrophages from the periphery, suppressed the proliferation of CNS microglia and infiltrated macrophage, facilitated the alternative activation (M2 state) of microglia/macrophages, and attenuated their ability to synthesize and release inflammatory cytokines. Conclusion: Our results suggest that inhibition of CX3CR1 signaling could function as a therapeutic modality in ischemic brain injury, by reducing recruitment of peripheral macrophages and expansion/activation of CNS microglia and macrophages, resulting in protection of neurological function. 

Retracted: No

PubPeer comments:
 image duplication, rotated ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Induction of nuclear translocation of constitutive androstane receptor by peroxisome proliferator-activated receptor alpha synthetic ligands in mouse liver
Authors: Janardan K Reddy
Yong Xu
Jeffrey M Peters
Jennifer E Foreman
Satdarshan P S Monga
Kasturi Haldar
Dongsheng Guo
Kojiro Matsumoto
Sonal Khare
Songtao Yu
Yuzhi Jia
M Sambasiva Rao
Kelly Suino-Powell
H Eric Xu
Joy Sarkar
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Peroxisome proliferators; nuclear receptor; peroxisome proliferator-activated receptor alpha; PPARalpha; synthetic ligands
Affiliations: Department of Pathology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois 60611-3008, USA.

Abstract:  Peroxisome proliferators activate nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha) and enhance the transcription of several genes in liver. We report here that synthetic PPARalpha ligands Wy-14,643, ciprofibrate, clofibrate, and others induce the nuclear translocation of constitutive androstane receptor (CAR) in mouse liver cells in vivo. Adenoviral-enhanced green fluorescent protein-CAR expression demonstrated that PPARalpha synthetic ligands drive CAR into the hepatocyte nucleus in a PPARalpha- and PPARbeta-independent manner. This translocation is dependent on the transcription coactivator PPAR-binding protein but independent of coactivators PRIP and SRC-1. PPARalpha ligand-induced nuclear translocation of CAR is not associated with induction of Cyp2b10 mRNA in mouse liver. PPARalpha ligands interfered with coactivator recruitment to the CAR ligand binding domain and reduced the constitutive transactivation of CAR. Both Wy-14,643 and ciprofibrate occupied the ligand binding pocket of CAR and adapted a binding mode similar to that of the CAR inverse agonist androstenol. These observations, therefore, provide information for the first time to indicate that PPARalpha ligands not only serve as PPARalpha agonists but possibly act as CAR antagonists. 

Retracted: No

PubPeer comments:
 The immunoblot for GAPDH in Fig 4A and 4B look like the results from the same sample. ![file] ,
Involvement of retinoblastoma (Rb) and E2F transcription factors during photodynamic therapy of human epidermoid carcinoma cells A431
Authors: N Ahmad
S Gupta
H Mukhtar
Journal: Oncogene (1999)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Photodynamic therapy; PDT; cancer cell-kill; mechanism; silicon phthalocyanine
Affiliations: Department of Dermatology, Case Western Reserve University, Cleveland, Ohio 44106, USA.

Abstract:  Photodynamic therapy (PDT), a promising new therapeutic modality for the management of a variety of solid malignancies and many non-malignant diseases, is a bimodal therapy using a porphyrin based photosensitizing chemical and visible light. The proper understanding of the mechanism of PDT-mediated cancer cell-kill may result in improving the efficacy of this treatment modality. Earlier we have shown (Proc. Natl. Acad. Sci. USA; 95: 6977-6982, 1998) that silicon phthalocyanine (Pc4)-PDT results in an induction of the cyclin kinase inhibitor WAF1/CIP1/p21 which, by inhibiting cyclins (E and D1) and cyclin dependent kinases (cdk2 and cdk6), results in a G0/G1-phase arrest followed by apoptosis in human epidermoid carcinoma cells A431. We have also demonstrated the generation of nitric oxide during PDT-mediated apoptosis (Cancer Res.; 58: 1785-1788, 1998). Retinoblastoma (pRb) and E2F family transcription factors are important proteins, which regulate the G1--&gt;S transition in the cell cycle. Here, we provide evidence for the involvement of pRb-E2F/DP machinery as an important contributor of PDT-mediated cell cycle arrest and apoptosis. Western blot analysis demonstrated a decrease in the hyper-phosphorylated form of pRb at 3, 6 and 12 h post-PDT with a relative increase in hypo-phosphorylated pRb. Western blot analysis also revealed that PDT-caused decrease in phosphorylation of pRb occurs at serine-780. The ELISA data demonstrated a time dependent accumulation of hypo-phosphorylated pRb by PDT. This response was accompanied with down-regulation in the protein expression of all five E2F (1-5) family transcription factors, and their heterodimeric partners DP1 and DP2. These results suggest that Pc4-PDT of A431 cells results in a down regulation of hyper-phosphorylated pRb protein with a relative increase in hypo-phosphorylated pRb that, in turn, compromises with the availability of free E2F. We suggest that these events result in a stoppage of the cell cycle progression at G1--&gt;S transition thereby leading to a G0/G1 phase arrest and a subsequent apoptotic cell death. These data provide an evidence for the involvement of pRb-E2F/DP machinery in PDT-mediated cell cycle arrest leading to apoptosis. 

Retracted: No

PubPeer comments:
 Figure 1. Much more similar than expected. https: imgur.com Vsutagv , 
 Figure 3. Much more similar than expected. https: imgur.com C9Dn0FN , 
 Figure 4. Much more similar than expected. https: imgur.com cGnWx2H ,
The medicinal fungus <em>Antrodia cinnamomea</em> regulates DNA repair and enhances the radiosensitivity of human esophageal cancer cells
Authors: Yu-Ming Liu
Yu-Jen Chen
Yu-Kuo Liu
Yu-Chuen Huang
Pin-I Huang
Tung-Hu Tsai
Ling-Wei Wang
Journal: OncoTargets and Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: G2/M; fermentation broth; mycelial; p21; radiosensitization.
Affiliations: Department of Oncology, Division of Radiation Oncology, Taipei Veterans General Hospital; School of Medicine, Institute of Traditional Medicine, National Yang Ming University, Taipei; School of Medicine, National Yang Ming University, Taipei., Department of Chemical and Material Engineering, Chang Gung University, Taoyuan City., Department of Oncology, Division of Radiation Oncology, Taipei Veterans General Hospital; School of Medicine, National Yang Ming University, Taipei., Department of Medical Research, China Medical University Hospital; School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung., School of Medicine, Institute of Traditional Medicine, National Yang Ming University, Taipei., School of Medicine, Institute of Traditional Medicine, National Yang Ming University, Taipei; Department of Radiation Oncology, MacKay Memorial Hospital, New Taipei City, Taiwan.

Abstract:  This study investigated the adjunctive effects of Antrodia cinnamomea mycelial fermentation broth (AC-MFB), a Taiwanese medicinal fungus, in enhancing the radiosensitivity of esophageal cancer cells. Human CE81T/VGH squamous and BE3 adenocarcinoma esophageal cancer cells were used in this study. A colony formation assay showed that pretreatment with AC-MFB decreased the survival of irradiated esophageal cancer cells, with a maximum sensitizer enhancement ratio of 1.91% and 37% survival. A DNA histogram study showed that AC-MFB pretreatment enhanced cell cycle arrest at the G2/M phase, the most radiosensitive phase. An immunofluorescence assay and a Western blotting assay showed that AC-MFB delayed the abrogation of γ-H2AX, upregulated p21 expression, and attenuated the radiation-induced phosphorylation of ataxia telangiectasia-mutated kinase and checkpoint kinase 2. An in vivo validation study showed that AC-MFB treatment tended to have a synergistic effect with radiation on the tumor growth delay of CE81T/VGH cells in BALB/c mice. These data suggest that this edible fungus product could enhance the effect of radiotherapy against esophageal cancer. 

Retracted: No

PubPeer comments:
 Two plots in Figure 3E appear to my eye to be the same. *** Closeup ![file] *** Full figure ![file] , 
 Some, but not all of the bands in Figure 5 appear to show evidence of splicing (green arrows). *** Closeup ![file] *** Full figure ![file] ,
Lead induces the up-regulation of the protein arginine methyltransferase 5 possibly by its promoter demethylation
Authors: Biji Chatterjee
Santosh R Kanade
Krishna Ghosh
Journal: Biochemical Journal (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DNMTs; MEP50; PRMT5; PRMT5 promoter; epigenetics
Affiliations: Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasargod, Kerala 671314, India

Abstract:  The studies on lead (Pb) exposure linking to epigenetic modulations are caused by its differential actions on global DNA methylation and histone modifications. These epigenetic changes may result in increased accessibility of the transcription factors to promoter DNA-binding elements leading to activation and expression of the gene. The protein arginine methyltransferase 5 (PRMT5) and its partner methylosome protein 50 (MEP50) together catalyze the mono- and symmetric dimethylation of arginine residues in many histone and non-histone protein substrates. Moreover, it is overexpressed in many forms of cancer. In the present study, the effects of Pb on the PRMT5 and MEP50 expression and formation of the symmetrically dimethylated arginine (SDMA), the catalytic product of the PRMT5-MEP50 complex were analyzed in vitro after exposing the A549 and MCF-7 cells. The results show that exposure to 0.1 and 1 µM of Pb strongly enhanced the expression of both PRMT5 and MEP50 transcript and protein leading to increased SDMA levels globally with H4R3 being increasingly symmetrically dimethylated in a dose-dependent manner after 48 h of Pb exposure in both cell types. The methylation-specific PCR also revealed that the CpG island present on the PRMT5 promoter proximal region was increasingly demethylated as the dose of Pb increased in a 48-h exposure window in both cells, with MCF-7 being more responsive to Pb-mediated PRMT5 promoter demethylation. The bisulfite sequencing confirmed this effect. The findings therefore indicate that Pb exposure increasing the PRMT5 expression might be one of the contributing epigenetic factors in the lead-mediated disease processes as PRMT5 has a versatile role in cellular functions and oncogenesis. 

Retracted: No

PubPeer comments:
 There is a a discontinuity in a Western immunoblot in Figure 3b. In Figure 4b, a blot has been duplicated, modified and presented as something else. This is seen by increasing the contrast and comparing the two blots. ![file] ,
Down-regulation of plant V-type H+-ATPase genes after light-induced inhibition of growth
Authors: R Viereck
R Low
T Rausch
M Kirsch
Journal: FEBS Letters (1996)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cell extension growth; vacuole enlargement; ER; Golgi vesicles; ion accumulation

Abstract:  Cell extension growth in the mesocotyl tip of dark-grown Zea mays L. seedlings is dependent on vacuole enlargement and massive flux of ER and Golgi vesicles. Water flow into the expanding vacuole is driven by ion accumulation, which in turn is energized by the vacuolar H+-ATPase (V-ATPase). The V-ATPase energizes the secondary ion transport into the expanding vacuole. As light exposure leads to a strong inhibition of extension growth, the effect of light on transcript levels for subunits A and c of the V-ATPase was analyzed. Partial homologous cDNAs for subunit A and two isoforms of subunit c were cloned by RT-PCR. In dark-grown seedlings transcript levels for both subunits were much higher in the growing mesocotyl tip than in the fully differentiated mesocotyl tissue. Only in the tip region did light exposure lead to a strong and coordinate down-regulation of both mRNAs whereas in the differentiated mesocotyl only a slight decrease was observed. The results indicate that expression of the 'housekeeping' V-type H+-ATPase is strongly regulated in response to growth rate. 

Retracted: No

PubPeer comments:
 Figure 3, really bizarre. ![file] , 
 #1 No, it isn t bizarre. It is common. And it shouldn t be too hard to figure out how it occurs. For many papers from the pre-digital era, subsequent digitization required scanning of the published version. While some journals used scanning methods that preserved as much information as possible, others did not (perhaps due to lack of resources), and used scans in which gray levels were lost and images became effectively black white. If you go to the FEBS Letters archives and look at any issue from 1996, you will find examples of this phenomenon in the majority of papers. Essentially, any image that was once a photograph is now either a black box or heavily over-contrasted. Line drawings are generally fine, of course. ,
Mice as a model for homeopathy research
Authors: Anisur Rahman Khuda-Bukhsh
Journal: Homeopathy (2009)
Discipline: CLINICAL MEDICINE
Keywords: Mice; homeopathy research; cytotoxicity; genotoxicity; carcinogenesis
Affiliations: Cytogenetics and Molecular Biology Laboratory, Department of Zoology, University of Kalyani, Kalyani 741235, West Bengal, India. 

Abstract:  Mice (Mus musculus) have been used as a model for homeopathy research in relation to cytotoxicity, genotoxicity and carcinogenesis in our laboratory for the last three decades. Initially, anti-radiation activities of several potentized homeopathic drugs were tested against suitable controls by taking into consideration several cytogenetic endpoints. Subsequently, anti-cytotoxic, anti-genotoxic and anti-oxidative stress effects of some homeopathic drugs were tested against several chemical toxic metalloids and metal compounds. Modern techniques including Western blot, immunofluorescence, electron microscopy, UV-spectroscopy, HPLC, FTIR, NMR, RT-PCR etc were deployed to understand the possible mechanisms and pathways of action of potentized homeopathic drugs. We hypothesise that one way by which potentized homeopathic drugs act is through regulatory action on gene expression. 

Retracted: No

PubPeer comments:
 Immunofluorescence Images in figure 3 appear to show areas of overlap. I did not carefully check elsewhere in the paper or figure. *** ![file] *** ![file] ,