PReD-Bench/PRed-Bench huggingface dataset:
Derricin and derricidin inhibit Wnt/β-catenin signaling and suppress colon cancer cell growth in vitro
Authors: Debora M Cerqueira
Felipe L Oliveira
Danilo Predes
Alice H Reis
Jose G Abreu
Fabio A Mendes
Marina C L Cayres
Barbara F Fonseca
Ricardo M Kuster
Nathalia G Amado
Journal: PloS one (2015)
Discipline: Multidisciplinary
Keywords: Wnt/β-catenin pathway; colorectal cancer; natural compounds; chalcone subclass; transcriptional inhibition
Affiliations: Universidade Federal do Rio de Janeiro, Instituto de Ciências Biomédicas, Rio de Janeiro, Brazil., Universidade Federal do Rio de Janeiro, Instituto de Pesquisas em Produtos Naturais, Rio de Janeiro, Brazil.

Abstract:  Overactivation of the Wnt/β-catenin pathway in adult tissues has been implicated in many diseases, such as colorectal cancer. Finding chemical substances that can prevent this phenomenon is an emerging problem. Recently, several natural compounds have been described as Wnt/β-catenin inhibitors and might be promising agents for the control of carcinogenesis. Here, we describe two natural substances, derricin and derricidin, belonging to the chalcone subclass, that show potent transcriptional inhibition of the Wnt/β-catenin pathway. Both chalcones are able to affect the cell distribution of β-catenin, and inhibit Wnt-specific reporter activity in HCT116 cells and in Xenopus embryos. Derricin and derricidin also strongly inhibited canonical Wnt activity in vitro, and rescued the Wnt-induced double axis phenotype in Xenopus embryos. As a consequence of Wnt/β-catenin inhibition, derricin and derricidin treatments reduce cell viability and lead to cell cycle arrest in colorectal cancer cell lines. Taken together, our results strongly support these chalcones as novel negative modulators of the Wnt/β-catenin pathway and colon cancer cell growth in vitro. 

Retracted: No

PubPeer comments:
 Fig. 4B might contain a duplication. Could the authors check please? ![file] Zoom: ![file] ,
The Collective Effect of MIP-3α and FL Promotes Dendritic Cell Function Within the Immune Microenvironment of Murine Liver Cancer
Authors: Xidong Chen
Chuanli Yang
Donglin Zhang
Haichao Zhao
Haoliang Zhao
Changzhou Chen
Yanjun Li
Jiefeng He
Journal: Frontiers in Oncology (2021)
Discipline: CLINICAL MEDICINE
Keywords: FL; MIP-3α; dendritic cells; hepatocellular carcinoma; tumor immune microenvironment.
Affiliations: Graduate School, Shanxi Medical University, Taiyuan, China., Department of Hepatobiliary Surgery, Shanxi Bethune Hospital Affiliated to Shanxi Medical University, Taiyuan, China.

Abstract:  Hepatocellular carcinoma is a highly malignant and lethal tumor. In addition to surgery, immunotherapy is currently a more effective treatment for hepatocellular carcinoma. The tumor immune microenvironment (TIME) largely determines the efficacy of cancer immunotherapy. Based on the universal targeting of TIME modulators in clinical treatment, TIME modulators are promising targets for tumor immunotherapy. We investigated the effect of a double gene expression vector (recombinant galactose-terminal glycol-poly-L-lysine coupled MIP-3α-FL) on dendritic cells (DCs) regulation within the TIME of mice with liver cancer. H22 cells were transfected with a recombinant MIP-3α-FL plasmid to induce DCs differentiation and chemotaxis. The effects of transfection were investigated by flow cytometry following the modified Boyden's method. Cytokine-induced killer (CIK) cells co-culture revealed changes in the antigen presentation ability of DCs. Further, tumor-bearing mice were injected with the recombinant double gene vector via the tail vein. We compared the survival time, tumor volume, weight of the mice, as well as the number and phenotype of tumor-infiltrating DCs (TIDCs) between groups. The supernatant of transfected H22 cells promoted the phenotypic maturation of DCs, enhancing their chemotaxis. Further, treated DCs promoted the cytokine secretion and killing ability of CIK cells. The survival time of mice injected with the double gene vector was significantly prolonged, while their tumor weight and volume were relatively reduced. Flow cytometry revealed that the number of TIDCs (as well as CD80 and CD86 expression) in the MouseMIP-3α-FL group, were significantly higher than in the control group. The combination of MIP-3α and FL can significantly promote DCs aggregation, maturation, and enhance their antigen presentation ability. The coupling of the double gene vector with glycosylated polylysine can improve the precise targeting of the liver and inhibit tumor growth in vivo, providing a novel approach for immune therapy in liver cancer. 

Retracted: Yes

PubPeer comments:
 Dear authors, Fig.5A contains multiple similar dot motifs in virtually all FACS dot plots. Could you please provide the original FCS files for review? ![file] , 
 **RETRACTED** https: www.frontiersin.org articles 10.3389 fonc.2021.744389 full ,
L-securinine induces apoptosis in the human promyelocytic leukemia cell line HL-60 and influences the expression of genes involved in the PI3K/AKT/mTOR signaling pathway
Authors: Maidong Li
Zhaoning Ji
Dongyun Chen
Gang Zhang
Shuwen Han
Wencai Ye
Ying Wang
Journal: Oncology reports (2014)
Discipline: CLINICAL MEDICINE
Keywords: Securinega alkaloids; apoptosis; antitumor drug; HL-60 cells; molecular mechanism
Affiliations: Department of Oncology, Wannan Medical College, Wuhu, Anhui, P.R. China., The Cancer Center, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui, P.R. China., Institute of Traditional Chinese Medicine and Natural Products, Jinan University, Guangzhou, P.R. China.

Abstract:  The Securinega alkaloids are a class of natural products isolated from plants of the Euphorbiaceae family. L-securinine induces apoptosis in the human promyelocytic leukemia cell line HL-60 indicating its potential as an efficient natural antitumor drug with low toxicity. The aim of the present study was to investigate the apoptotic effects of L-securinine on HL-60 cells and to explore its potential underlying molecular mechanism(s) as an antitumor agent. HL-60 cells were cultured with L-securinine. The proliferation and changes in cell morphology were evaluated by cell counting Kit-8 (CCK-8) assay and electron microscopy, respectively. Induction of apoptosis and cell cycle progression were investigated by flow cytometry. The PI3K/AKT/mTOR pathway gene expression was measured by quantitative PCR (qPCR). L-securinine decreased the viability of HL-60 cells in a dose- and time-dependent manner, with IC50 values at 24, 48 and 72 h post-treatment of 47.88, 23.85 and 18.87 µmol/l, respectively. Numerous apoptotic bodies were observed in the HL-60 cells treated with 25 µmol/l L-securinine for 48 h. L-securinine at 12.5, 25 and 50 µmol/l increased the rate of apoptosis in HL-60 cells, and G1/S phase progression was retarded. Furthermore, L-securinine induced downregulation of PI3K, AKT and mTOR gene expression and upregulation of PTEN gene expression in a dose-dependent manner. In conclusion, L-securinine induces apoptosis and inhibition of cell cycle progression in HL-60 cells by modulation of the PI3K/AKT/mTOR pathway gene expression. These observations indicate the potential of L-securinine as an antitumor agent. 

Retracted: No

PubPeer comments:
  Figure 6 - Flow cytometric analysis of apoptosis in HL-60 cells following treatment with L-securinine. Apoptotic cell rates using FACS scan following L-securinine treatment in HL-60 cells. (A) Negative control HL-60 cells. HL-60 cells treated with (B) 12.5, (C) 25.0 and (D) 50.0 u03bcM of L-securinine for 48 h, respectively. All the points present in (A) are also present in (B). In turn, all the points in (B) are also visible in (C), along with additional cells. All three panels are subsets of the same experimental data. ![file] ,
De novo epileptic confusion in the elderly: a 1-year prospective study
Authors: Laurent Vercueil
Olivier Veran
Pierre Thomas
Sophie Hamelin
Cecile Sabourdy
Philippe Kahane
Journal: Epilepsia (2009)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Nonconvulsive status epilepticus; NCSE; elderly patients; confusion of unknown origin; EEG
Affiliations: Neurology Clinic, University Hospital, Grenoble, France. 

Abstract:  Purpose: Nonconvulsive status epilepticus (NCSE) is clinically difficult to diagnose, especially in old patients without epilepsy, and requires electroencephalography (EEG) for diagnosis. Its incidence among elderly patients with confusion of unknown origin (CUO) remains undetermined. Methods: A 1-year prospective study was conducted in patients aged 60 years or older, for whom EEG was requested because of confusion considered to be of unknown origin after initial clinical, biologic, and imaging investigations. Diagnosis criteria included a validated clinical assessment scale to confirm confusion. Results: Of 44 patients with confirmed CUO, 7 presented with de novo NCSE. NCSE population had a mean age of 76 years (range, 60-97 years). No statistically significant differences were found between NCSE patients and others for age, drugs, presence of myoclonia, eyelid myoclonia, tachycardia, or agitation. In contrast, an acute onset (&lt;24 h), gender (100% female among NCSE patients), and lack of clinical response to simple commands were significantly associated with NCSE. No differences between the two groups were evidenced for mortality and morbidity (length of hospitalization, social outcome, and so on). Discussion: Almost 16% of patients aged 60 or older with confusion of unknown origin had NCSE, according to this first prospective study. Female patients with rapid onset (&lt;24 h) of symptoms and lack of response to simple commands were at a higher risk of presenting with NCSE. 

Retracted: No

PubPeer comments:
 While reading this paper, I have problem for interpretation of brain CT. The authors did not explain how they read this radiological examination in the section patients and methods. So we don t know the criteria they used for assessing abnormal images. ![file] First, I guess that rapid onset is not related to brain CT. Normal CT is present in 43% of patients (first column) and 33% of patients (second column) Abnormal CT is present in 71% of patients (first column) and 76% of patients (second column) The total is superior to 100%. Furthermore, could the authors explain what are sequelae? ,
Hispolon inhibits breast cancer cell migration by reversal of epithelial-to-mesenchymal transition via suppressing the ROS/ERK/Slug/E-cadherin pathway
Authors: Yong-Quan Li
Yi-Sheng Sun
Long-Xian Lv
Wei Chen
Zhao Zhao
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: Hispolon; anticancer effects; breast cancer cells; anti-migration activity; cellular ROS
Affiliations: Centre of Laboratory Medicine, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, P.R. China., College of Life Science, Zhejiang University, Hangzhou, Zhejiang, P.R. China.

Abstract:  Hispolon has been shown to have anticancer effects on various tumors. However, whether hispolon exerts anti-migration activity in breast cancer cells and the underlying mechanisms, have not been elucidated yet. In the present study, our data demonstrated that hispolon inhibited TPA-induced breast cancer MCF-7 cell migration at sub-toxic concentrations in vitro. Hispolon decreased the level of cellular ROS significantly and repressed TPA-induced phosphorylation of extracellular signal-regulated kinase (ERK), accompanied by upregulation of E-cadherin and downregulation of the transcriptional repressor Slug. Furthermore, N-acetyl-cysteine, an antioxidant agent, markedly suppressed TPA-induced epithelial-to-mesenchymal transition, cell migration and activation of ERK. Taken together, our results indicated that hispolon suppressed the migration of breast cancer cells via suppressing the ROS/ERK/Slug/E‑cadherin pathway. Hispolon may be developed as a potential antimetastasis agent to breast cancer. 

Retracted: No

PubPeer comments:
 Figure 7. * Red boxes: The  TPA and  TPA + U0126 panels appear to look very similar ![file] ,
HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
Authors: Yong-Heng Bai
Peng Xia
Hai-Cong Zhang
Jian-Jian Zheng
Cun-Zao Wu
Yong Guo
Journal: OncoTargets and Therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: HMGB1; RCC; angiogenesis; apoptosis; autophagy
Affiliations: Department of Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China, ., Department of Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., Department of Pathology, The Fifth Hospital of Shijiazhuang, Shijiazhuang, China.

Abstract:  Background: High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers. Methods: CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively. Results: In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth. Conclusion: Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC. 

Retracted: No

PubPeer comments:
 There was an overlap in Figure 3. We found an original paper in https: kns.cnki.net kcms detail detail.aspx?dbcode=CDFD dbname=CDFDLAST2019 filename=1019867621.nh uniplatform=NZKPT v=gNG99WHe6Zh3JhnXeN-dAa1OJuOya-rXU6KI1w5OdSPTASUjcG-kEpkGHYpy2Lrt. The original paper is a paper for doctoral degree. We also found the overlap in figure. ![file] ![file] ![file] ![file] , 
 The result of flow cytometry assay was different between this paper and original paper, but they are the identical experiment. ![file] ![file] The result of flow cytometry assay in original paper is as follows. ![file] ![file] , 
 There was no western blot analysis of p62 in original paper. ![file] ![file] The result of western blotanalysis in original paper is as follows. ![file] ![file] ,
Receptors for advanced glycation end products is associated with autophagy in the clear cell renal cell carcinoma
Authors: Hai-Cong Zhang
Jun-Hua Zheng
Yong Guo
Sheng Xue
Journal: Journal of cancer research and therapeutics (2019)
Discipline: CLINICAL MEDICINE
Keywords: Autophagy; clear cell renal cell carcinoma; high-mobility group box 1; receptor for advanced glycation end-product.
Affiliations: Department of Urology, Shanghai Tenth People's Hospital of Nanjing Medical University, Nanjing; Transplantation Centre, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., Department of Pathology, The Fifth Hospital of Shijiazhuang, Shijiazhuang, China., Department of Urology, Shanghai Tenth People's Hospital of Nanjing Medical University, Nanjing, China., Department of Urology, Shanghai General Hospital of Nanjing Medical University, Nanjing; Department of Urology, The Affiliated First People's Hospital of Shanghai Jiao Tong University, Shanghai, China.

Abstract:  Background: The receptor for advanced glycation end-product (RAGE) was one of the signal transduction receptors. RAGE interacted with various signaling molecules which were involved in human disease processes including tumorigenesis. Previous reports have indicated that RAGE/high-mobility group box 1 (HMGB1) could regulate autophagy in different carcinomas. However, the functional role of RAGE/ HMGB1 in the regulation of clear cell renal cell carcinoma (ccRCC) autophagy remained unrevealed. Methods: Western blot, quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence were used in the present study. Results: In this study, we demonstrated that the levels of RAGE/HMGB1 and autophagic protein LC3, Beclin-1, PI3K were much higher in ccRCC samples than those of in adjacent normal tissues. RAGE and autophagic protein expression was regulated with RAGE/HMGB1 in human RCC cell lines. Conclusion: Our results implicated that RAGE and autophagy played important roles in ccRCC, and RAGE/HMGB1 might serve as a novel therapeutic target for future ccRCC treatment. 

Retracted: No

PubPeer comments:
 In figure 1, the backgrounds of RAGE and PI3K are different from others. It seems that they were not retrieved from the same gel and membrane. ![file] ,
Role of CC-chemokine receptor 5 on myocardial ischemia–reperfusion injury in rats
Authors: Bo Yang
Ling Gao
Bo Shen
Jieyu Zhang
Jun Li
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CCR5; myocardial ischemia-reperfusion injury; inflammatory response; myocardial infarction; NF-κB
Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.

Abstract:  The expression level of CC-chemokine receptor 5 (CCR5) is enhanced post inflammatory stimulations and might play a crucial role on inflammatory cells infiltration post myocardial ischemia. The purpose of this study was to evaluate the role of CCR5 on myocardial ischemia-reperfusion (I/R) injury in rats. Adult male rats were randomized to sham group, I/R group (I/R, 30 min coronary artery occlusion followed by 2-h reperfusion), ischemic preconditioning (I/R + Pre), CCR5 antibody group [I/R + CCR5Ab (0.2 mg/kg)], and CCR5 agonist group [I/R + CCR5Ago, RNATES (0.1 mg/kg)], n = 12 each group. The serum level of creatine kinase (CK) and tumor necrosis factor α (TNF-α) were measured by ELISA. Myocardial infarction size and myeloperoxidase (MPO) activity were determined. Myocardial protein expression of CCR5 and intercellular adhesion molecule-1 (ICAM-1) were evaluated by Western blotting and immunohistochemistry staining, respectively. Myocardial nuclear factor-kappa B (NF-κB) activity was assayed by electrophoretic mobility shift assay. Myocardial CCR5 protein expression was significantly reduced in I/R + Pre group (P &lt; 0.05 vs. I/R) and further reduced in I/R + CCR5Ab group (P &lt; 0.05 vs. I/R + Pre). LVSP and ±dP/dt(max) were significantly lower while serum CK and TNF-α as well as myocardial MPO activity, ICAM-1 expression, and NF-κB activity were significantly higher in I/R group than in sham group (all P &lt; 0.05), which were significantly reversed by I/R + Pre (all P &lt; 0.05 vs. I/R) and I/R + CCR5Ab (all P &lt; 0.05 vs. I/R + Pre) while aggravated by I/R + CCR5Ago (all P &lt; 0.05 vs. I/R). Our results suggest that blocking CCR5 attenuates while enhancing CCR5 aggravates myocardial I/R injury through modulating inflammatory responses in rat heart. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: Two panels appear to overlap Figure 5. * Blue boxes: Two panels appear to overlap Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. I would love to hear from the authors if the journal ever contacted them in the past five years. ![file] ,
New insights on the modulatory roles of metformin or alpha-lipoic acid versus their combination in dextran sulfate sodium-induced chronic colitis in rats
Authors: Samah M Elaidy
Mohammad S Hassan
Soha S Essawy
Fatma S Samman
Journal: Pharmacological Reports (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Alpha-lipoic acid; Dextran sulfate sodium-induced chronic colitis; Metformin; Nuclear factor-kappa-B; Oxidative stress.
Affiliations: Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, Egypt., Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, Egypt. Electronic address: .

Abstract:  Background: Dextran sulfate sodium (DSS)-induced colitis is the most widely used model that resembles ulcerative colitis (UC) in human with challenging chronic mechanistic oxidative stress-inflammatory/immunological cascades. In models of acute colitis, reduction of oxidative stress and inflammatory burdens beside manipulation of many transcriptional factors were achieved by metformin or alpha-lipoic acid (α-LA). Currently, in vivo DSS-induced chronic colitis was conducted and the possible therapeutic roles of metformin and/or α-LA were explored. Methods: Chronic UC was induced by adding 5% DSS orally in drinking water for 7days followed by 3% DSS in drinking water for 14days in adult male albino Wistar rats. Intraperitoneal administration of α-LA (25mg/kg, twice/day) and/or metformin (100mg/kg/day) were set at day 7 of DSS administration and continued for 14days. Body weights, survival rates, disease activity index (DAI), colonic oxidative stress markers, tumor necrosis factor (TNF)-α levels, colonic nuclear factor-kappa-B (NF-κB) immunohistochemical expression, and the colonic histopathological changes were observed. Results: Metformin or/and α-LA attenuated the severity of the DSS-induced colitis through improving the reductions in body weights, the DAI, the colonic oxidative stress markers, TNF-α, and NF-κB levels, and the morphological mucosal damage scores. Significant synergetic therapeutic effects were observed with combined therapeutic regimens. Conclusion: Therapeutically, metformin and α-LA could be administered in chronic colitis. The combination of currently used pharmaceutics with natural and synthetic potent antioxidant compounds will become a therapeutic strategy of choice for UC to improve the quality of life if sufficient clinical trials are available. 

Retracted: No

PubPeer comments:
 Another case of apparently repeated features within images (blue boxes) from this group. The surrounding tissue is not readily obvious as the same. *** ![file] *** Full figure ![file] ,
Modulatory effect of Ganoderma lucidum on expression of xenobiotic enzymes, oxidant-antioxidant and hormonal status in 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma in rats
Authors: Krishnamoorthy Deepalakshmi
Sankaran Mirunalini
Journal: Pharmacognosy magazine (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: 12-dimethylbenz(a)anthracene; 7; Antioxidant; Ganoderma lucidum; mammary cancer

Abstract:  Background: Mushrooms are an important natural source represents a major and untapped potent pharmaceutical product. Ganoderma lucidum (G. lucidum) an important medicinal mushroom has been shown to contain high amount of antioxidant. However, in vivo studies on G. lucidum fruiting bodies are lacking. Objectives: To determine the effects of G. lucidum fruiting bodies ethanolic extract (GLEet) on expression of xenobiotic enzymes, oxidant-antioxidant and hormonal status on 7,12-dimethyl benz[a]antheracene (DMBA) induced experimental breast cancer was investigated in female Sprague dawley rats. Materials and methods: Cancer bearing female Sprague dawley rats was orally treated with GLEet (500mg/kg body weight) for 16 weeks. Incidence and tumor volume in each groups, and biochemical parameters were carried out in plasma, liver, and mammary tissues of animals. Histopathological and immunohistochemical analysis were also determined. Result: Oral administration of GLEet on tumor bearing animals significantly diminished the levels of lipid peroxidation thereby enhancing the nonenzymatic antioxidants and also positively regulated the estrogen receptor hormones level to near normal when compared with DMBA treated rats. Moreover, it also positively modulates the xenobiotic metabolizing enzymes. Therefore, the dietary administration of G. lucidum may be efficiently used as a chemopreventive agent against mammary carcinogenesis. Conclusion: We concluded that G. lucidum is a potent chemopreventive agent, thereby it offers maximum protection against DMBA-induced mammary carcinogenesis. 

Retracted: No

PubPeer comments:
 Concern about Figure 4. Panels a (control) and d (control + GLEet) appear to show a very similar sample, albeit 90 degrees rotated. Shown with red boxes. , 
 Figure 4 highlighted: ![file] , 
 Concern about Figure 5. Panels a (control) and d (control + GLEet) appear to show a very similar sample, albeit 90 degrees rotated. Shown with blue boxes. ![file] ,
RETRACTED ARTICLE: α2,6-Sialylation mediates hepatocellular carcinoma growth in vitro and in vivo by targeting the Wnt/β-catenin pathway
Authors: S Wang
H Zhang
Q Yuan
A Wei
X Chen
Y Zhao
X Yu
L Wang
J Zhang
Journal: Oncogenesis (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Abnormal sialylation; sialyltransferases; tumorigenesis; tumor progression; ST6Gal-I
Affiliations: Department of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Liaoning Province, China., School of Life Science and Medicine, Dalian University of Technology, Liaoning Province, China., Department of Pathology, Dalian Medical University, Liaoning Province, China.

Abstract:  Abnormal sialylation due to overexpression of sialyltransferases has been associated with tumorigenesis and tumor progression. Although ST6Gal-I influences cancer persistence and progression by affecting various receptors, the underlying mechanisms and mediators remain largely obscure, especially in hepatocellular carcinoma (HCC). We found that ST6Gal-I expression was markedly upregulated in HCC tissues and cells, high levels being associated with aggressive phenotype and poor prognosis. Furthermore, we examined the roles and mechanisms of ST6Gal-I in HCC tumorigenesis and metastasis in vitro and in vivo. ST6Gal-I overexpression promoted proliferation, migration and invasion of Huh-7 cells, whereas its knockdown restricted these abilities in MHCC97-H cells. Additionally, in a mouse xenograft model, ST6Gal-I-knockdown MHCC97-H cells formed significantly smaller tumors, implying that ST6Gal-I overexpression can induce HCC cell malignant transformation. Importantly, enhanced HCC tumorigenesis and metastasis by ST6Gal-I may be associated with Wnt/β-catenin signaling promotion, including β-catenin nuclear transition and upregulation of downstream molecules. Together, our results suggest a role for ST6Gal-I in promoting the growth and invasion of HCC cells through the modulation of Wnt/β-catenin signaling molecules, and that ST6Gal-I might be a promising marker for prognosis and therapy of HCC. 

Retracted: Yes

PubPeer comments:
 Above: Fig 7,  Fluorescence photomicrograph of **inflamed joint tissue** sac after 45-min administration of FITC labelled (A) plain drug solution, **(B) ETX-NPs and (C) F-ETX-NPs**. Below: Fig. 8 from [Jain et al (2015)] ,  Fluorescence photomicrograph of **liver tissue** sac after 45-min administration of FITC labeled a plain drug solution, **b N-SucCSNP**, and **c Lac-N-Suc-CSNP** . ![file] , 
 #1 See also Figure 6 from [Mishra et al (2014)] ,  Fluorescent photograph of FITC-labelled (a) plain drug solution, (b) chitosan nanoparticles and (c) glycyrrhizin conjugated low molecular weight chitosan nanoparticles in **liver sac**. ![] (c) is recognisable as the same thoughout (though not compressed horizontally in the Mishra version). The Mishra (a) and (b) appear to be blurred-out versions of (a) and (b) in the companion papers. ![] ,
Combined inhibitory effects of green tea polyphenols and selective cyclooxygenase-2 inhibitors on the growth of human prostate cancer cells both in vitro and in vivo
Authors: Deeba Nadeem Syed
Sami Sarfaraz
Najia Zaman
Vaqar Mustafa Adhami
Farrukh Afaq
Farrukh Sierre Pasha
Mohammad Saleem
Hasan Mukhtar
Imtiaz Ahmad Siddiqui
Arshi Malik
Journal: Clinical Cancer Research (2007)
Discipline: CLINICAL MEDICINE
Keywords: COX-2 inhibitors; chemoprevention; EGCG; prostate cancer cells; apoptosis
Affiliations: Department of Dermatology, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.

Abstract:  Purpose: Cyclooxygenase-2 (COX-2) inhibitors hold promise for cancer chemoprevention; however, recent toxicity concerns suggest that new strategies are needed. One approach to overcome this limitation is to use lower doses of COX-2 inhibitors in combination with other established agents with complementary mechanisms. In this study, the effect of (-)epigallocatechin-3-gallate (EGCG), a promising chemopreventive agent from green tea, was tested alone and in combination with specific COX-2 inhibitors on the growth of human prostate cancer cells both in vitro and in vivo. Experimental design: Human prostate cancer cells LNCaP, PC-3, and CWR22Rnu1 were treated with EGCG and NS398 alone and in combination, and their effect on growth and apoptosis was evaluated. In vivo, athymic nude mice implanted with androgen-sensitive CWR22Rnu1 cells were given green tea polyphenols (0.1% in drinking water) and celecoxib (5 mg/kg, i.p., daily, 5 days per week), alone and in combination, and their effect on tumor growth was evaluated. Results: Combination of EGCG (10-40 micromol/L) and NS-398 (10 micromol/L) resulted in enhanced (a) cell growth inhibition; (b) apoptosis induction; (c) expression of Bax, pro-caspase-6, and pro-caspase-9, and poly(ADP)ribose polymerase cleavage; (d) inhibition of peroxisome proliferator activated receptor gamma; and (e) inhibition of nuclear factor-kappaB compared with the additive effects of the two agents alone, suggesting a possible synergism. In vivo, combination treatment with green tea polyphenols and celecoxib resulted in enhanced (a) tumor growth inhibition, (b) lowering of prostate-specific antigen levels, (c) lowering of insulin-like growth factor-I levels, and (d) circulating levels of serum insulin-like growth factor binding protein-3 compared with results of single-agent treatment. Conclusions: These data suggest synergistic and/or additive effects of combinatorial chemopreventive agents and underscore the need for rational design of human clinical trials. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than expected. https: imgur.com t4y3nG5 ,
Diverticular Disease of the Colon: Neuromuscular Function Abnormalities
Authors: Gabrio Bassotti
Nunzia Bernardini
Maria P Dore
Vincenzo Villanacci
Journal: Journal of Clinical Gastroenterology (2016)
Discipline: CLINICAL MEDICINE
Keywords: Colonic diverticular disease; pathophysiological mechanisms; concomitant factors; anatomic abnormalities; functional abnormalities
Affiliations: *Gastroenterology and Hepatology Section, Department of Medicine, University of Perugia Medical School, Perugia †Pathology Section, Spedali Civili, Brescia ‡Histology and Medical Embryology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa §Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy.

Abstract:  Colonic diverticular disease is a frequent finding in daily clinical practice. However, its pathophysiological mechanisms are largely unknown. This condition is likely the result of several concomitant factors occurring together to cause anatomic and functional abnormalities, leading as a result to the outpouching of the colonic mucosa. A pivotal role seems to be played by an abnormal colonic neuromuscular function, as shown repeatedly in these patients, and by an altered visceral perception. There is recent evidence that these abnormalities might be related to the derangement of the enteric innervation, to an abnormal distribution of mucosal neuropeptides, and to low-grade mucosal inflammation. The latter might be responsible for the development of visceral hypersensitivity, often causing abdominal pain in a subset of these patients. 

Retracted: No

PubPeer comments:
 ![file] ![file] ![file] ![file] ![file] , 
 More images duplications in these three papers. Images were used to illustrate patients with Crohn disease, Slow transit constipation and diverticular disease. As needed by the circumstance. ![file] ![file] ![file] , 
 The same images were reused three times as a purpotted representation of patients with slow transit constipation, but also for diverticular disease. ![file] ,
Epigenome rejuvenation: HP1β mobility as a measure of pluripotent and senescent chromatin ground states
Authors: Maria Manukyan
Prim B Singh
Journal: Scientific Reports (2014)
Discipline: Multidisciplinary
Keywords: HP1β; epigenetic modifier; FRAP; human cells; differentiation
Affiliations: Albert-Ludwigs-Universität Freiburg, BIOSS Centre for Biological Signalling Studies, Schänzlestrasse 18, 79104 Freiburg, Germany., Fächerverbund Anatomie, Institut für Zell- und Neurobiologie, Charite - Universitätsmedizin, 10117 Berlin, Germany.

Abstract:  We measured the dynamics of an essential epigenetic modifier, HP1β, in human cells at different stages of differentiation using Fluorescence Recovery After Photobleaching (FRAP). We found that HP1β mobility is similar in human embryonic stem cells (hES) and iPS cells where it is more mobile compared to fibroblasts; HP1β is less mobile in senescent fibroblasts than in young (dividing) fibroblasts. Introduction of "reprogramming factors", Oct4, Sox2, Klf4, cMyc and Lin28, into senescent fibroblasts and measuring the changes in HP1β mobility as reprogramming proceeds shows that the mobility of HP1β in senescent cells increases and by day 9 is the same as that found in young fibroblasts. Thus the dynamics of a key epigenetic modifier can be rejuvenated without de-differentiation through an embryonic stage. Future work will test whether other aspects of cellular physiology that age can be so rejuvenated without de-differentiation. 

Retracted: No

PubPeer comments:
 Discussion regarding this article in another Pubpeer thread:  So in conclusion, Manukyan and Singh (2014) may have wanted to test their hypothesis but the model they used was not strong enough to support the conclusions (because again, in vitro induced senescence of embryonic fibroblasts is not a model of aging). https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#10 , 
 #1 The conclusion drawn is, in fact, precisely the opposite if one reads the entire exchange, especially: https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#11, https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#18 and https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#19 Comments made by https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#10 may be related to https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#6 and https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#14. , 
 Well done Manukyan and Singh - the first demonstration of rejuvenation without de-differentiation. see https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A#22 ,
Onzin, a c-Myc-repressed target, promotes survival and transformation by modulating the Akt–Mdm2–p53 pathway
Authors: Kristi Rothermund
Simon Watkins
Edward V Prochownik
Kenneth Rogulski
Youjun Li
Lixia Pu
Fenghua Yi
Journal: Oncogene (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: c-Myc; onzin; transcription factor; myeloid cells; growth rate
Affiliations: Section of Hematology/Oncology, Children's Hospital of Pittsburgh, Pittsburgh, PA 15213, USA.

Abstract:  The c-Myc oncoprotein is a general transcription factor whose target genes dictate the c-Myc phenotype. One such target of c-Myc, 'onzin', is normally expressed at high levels in myeloid cells and is dramatically downregulated in response to c-Myc overexpression. We show here that short hairpin interfering RNA-mediated knockdown of endogenous onzin results in a reduced growth rate and a proapoptotic phenotype. In contrast, onzin overexpression in fibroblasts is associated with an increased growth rate, resistance to apoptotic stimuli, loss of the G2/M checkpoint, and tumorigenic conversion. Onzin-overexpressing cells fail to induce p53 in response to apoptotic stimuli and contain higher levels of the active, phosphorylated forms of Akt1 and, more strikingly, of Mdm2. Using yeast two-hybrid and coimmunoprecipitation assays, we show that onzin directly interacts with both proteins. Green fluorescent protein tagging also confirms directly that Akt1 and Mdm2 colocalize with onzin, although the precise subcellular distribution of each protein is dependent on its relative abundance. Collectively, our results identify onzin as a novel regulator of several p53-dependent aspects of the c-Myc phenotype via its dramatic effect on Mdm2. This is reminiscent of the c-Myc --&gt; p19(ARF)--mid R: Mdm2 pathway and might function as a complementary arm to ensure the proper cellular response to oncogenic and/or apoptotic stimuli. 

Retracted: No

PubPeer comments:
 Figure 4b. Much more similar than expected. https: imgur.com IM44Lfi ,
Long non-coding RNA HEIH modulates CDK8 expression by inhibiting miR-193a-5p to accelerate nasopharyngeal carcinoma progression
Authors: Z-Y Song
S-X Wang
Y-E Han
J-M Tao
X Ju
Journal: European review for medical and pharmacological sciences (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Nasopharyngeal carcinoma; lncRNA HEIH; miR-193a-5p; CDK8; cell proliferation
Affiliations: Department of Otorhinolaryngology, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, China. .

Abstract:  Objective: Nasopharyngeal carcinoma (NPC) is the commonest malignant tumor. In this article, we aimed to examine the molecular role of lncRNA HEIH in the progression of NPC. Patients and methods: We assessed the expression of HEIH, miR-193a-5p and CDK8 in NPC tissues and cells by real-time PCR. The cell proliferation, invasion and migration of SUNE-1 cells were examined by CCK-8 and transwell assay. Western blot assay was adopted to measure the protein expression level of CDK8. Dual-Luciferase reporter assay was adopted to evaluate the correlation between HEIH, miR-193a-5p and CDK8. Results: We discovered that HEIH was high expressed and miR-193a-5p was reduced in both NPC tissues and cells. The upregulation of HEIH facilitated cell proliferation, migration and invasion of SUNE-1 cells. In addition, overexpression of miR-193a-5p restrained cell progression of SUNE-1 cells. Moreover, HEIH was proved to be a molecular sponge of miR-193a-5p in NPC. Besides that, CDK8 was found to be a direct target gene of miR-193a-5p in NPC. Furthermore, CDK8 knockdown suppressed cell progression of SUNE-1 cells. Conclusions: Our data demonstrated that HEIH overexpression promoted cell progression by sponging miR-193a-5p and upregulating CDK8. 

Retracted: No

PubPeer comments:
 The authors claim to have grown a so called Cd2+ influenced potassium acid phthalate single crystal for photonic device applications as can be evidenced from the first sentence of the abstract  *A very first attempt has been made to improve the overall performance of potassium hydrogen phthalate (KAP) crystal using Cd2+ ion*, . This appears to be another questionable claim from the groups of Anis Hussaini. However it is not clear what does one mean by Cd2+ influenced KAP crystal and if this is the same (or different) from a Cd2 doped KAP. Authors are requested to clarify this and also explain as to how Cd+2 (dication) will influence the structure of a monocationic K+ metal and will there not be any charge imbalance. Authors may like to clarify as to how Cd+2 will influence the crystal. ,
Propofol suppresses proliferation and invasion of glioma cells by upregulating microRNA-218 expression
Authors: Weiyun Xu
Jinquan Xu
Jiaqun Zhu
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: Propofol; Glioma cells; Proliferation; Invasion; Apoptosis
Affiliations: Department of Anesthesiology, Jinhua Municipal Central Hospital, Jinhua, Zhejiang 321000, P.R. China.

Abstract:  Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent. The present study aimed to assess the effect of propofol on the proliferation and invasion of human glioma cells, and to determine the potential underlying molecular mechanisms. The effects of propofol on U373 glioblastoma cell proliferation, apoptosis and invasion were detected by an MTT assay, caspase‑3 activity measurement and a Matrigel™ invasion assay, respectively. MicroRNA (miR)‑218 expression and matrix metalloproteinase (MMP)‑2 protein expression levels were analyzed by quantitative polymerase chain reaction and western blot analysis, respectively. In addition, miR‑218 precursor was transfected into the cells to assess whether overexpression of miR‑218 could affect MMP‑2 expression. Anti‑miR‑218 was transfected into the cells to evaluate the role of miR‑218 in the effects of propofol on the biological behavior of glioma cells. The results of the present study demonstrated that propofol significantly increased the expression levels of miR‑218, inhibited U373 cell proliferation and invasion, and facilitated apoptosis. In addition, treatment with propofol efficiently reduced MMP‑2 protein expression levels, and overexpression of miR‑218 also decreased MMP‑2 protein expression levels. Whereas, neutralization of miR‑218 using the anti‑miR-218 antibody reversed the effects of propofol on the biological behavior of U373 cells, and on the inhibition of MMP-2 protein expression. In conclusion, propofol may effectively suppress proliferation and invasion, and induce the apoptosis of glioma cells, at least partially through upregulation of miR-218 expression. 

Retracted: No

PubPeer comments:
 *[left]* Fig 1B.  Hoechst 33258 staining demonstrated promoted U373 cell apoptosis following propofol stimulation . *[middle]* Fig 2B from [Ye et al (2014)] .  Propofol inhibits cell proliferation, promotes apoptosis, and reduces invasion. Propofol treatment... promoted apoptosis (B and C) ... of osteosarcoma cell line MG63 in a dose-dependent manner . Image brightened for clarity. *[right]* Fig 2B from [Wang et al (2015)] .  Propofol inhibits cell proliferation, promotes apoptosis, and reduces invasion. Propofol treatment ...promoted apoptosis (B and C) ... of the pancreatic cancer cell line Panc-1 in a dose-dependent manner . From the Department of Unexpected similarities. ![file] , 
 #1 *[left]* Fig 5C. *[middle]* Fig 6C from [Ye et al (2014)] . Image brightened for clarity. *[right]* Fig 4C from [Wang et al (2015)] . ![file] ,
Prior Knowledge Driven Joint NMF Algorithm for ceRNA Co-Module Identification
Authors: Wei Kong
Xiaoyang Mou
Shuaiqun Wang
Jin Deng
Weiming Zeng
Journal: International journal of biological sciences (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ceRNA; lncRNA; mRNA; miRNA; tumor.
Affiliations: College of Information Engineering, Shanghai Maritime University, 1550 Haigang Ave., Shanghai 201306, P. R. China., Department of Biochemistry, Rowan University and Guava Medicine, Glassboro, New Jersey 08028, USA.

Abstract:  MRNA and lncRNA serve as a type of endogenous RNA in cell, which can competitively bind to the same miRNA through miRNA response elements (MREs), thereby regulating their respective expression levels, playing an important role in post-transcriptional regulation, and regulating the progress of tumors. The proposed competing endogenous RNA (ceRNA) hypothesis provides novel clues for the occurrence and development of tumors, but the integrative analysis methods of diverse RNA data are significantly limited. In order to find out the relationship among miRNA, mRNA and lncRNA, the previous studies only used individual dataset as seeds to search two other related data in the database to construct ceRNA network, but it was difficult to identify the synchronized effects from multiple regulatory levels. Here, we developed the joint matrix factorization method integrating prior knowledge to map the three types of RNA data of lung cancer to the common coordinate system and construct the ceRNA network corresponding to the common module. The results show that more than 90% of the modules are closely related to cancer, including lung cancer. Furthermore, the resulting ceRNA network not only accurately excavates the known correlation of the three types of RNA molecular, but also further discovers the potential biological associations of them. Our work provides support and foundation for future biological validation how competitive relationships of multiple RNAs affects the development of tumors. 

Retracted: No

PubPeer comments:
 (a) According to the title, the u201c**ashy**u201d neural network is applied in this paper. However, according to the abstract and Section 2, it seems that u201c**grey**u201d neural network is the more formal term. (b) Some unrelated papers are cited in the text. For example, it is claimed in Section 1 that u201cIn the 1970 s, the A7E attack aircraft engine monitoring system could be called the earliest PHM prototype [5u20137].u201d However, **ref[5-7] have nothing to do with engine monitoring.** ![file] ![file] ![file] ![file] ,
WITHDRAWN: Novel long-acting BF-30 conjugate corrects pancreatic carcinoma via cytoplasmic membrane permeabilization and DNA-binding in tumor-bearing mice
Authors: Ludong Tan
Zhe Jin
Baoxing Jia
Qingmin Chen
Yahui Liu
Journal: Life Sciences (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: withdrawn; editor request; Publisher; inconvenience; Elsevier Policy
Affiliations: The First Hospital of Jilin University, Changchun, Jilin 130021, China., The First Hospital of Jilin University, Changchun, Jilin 130021, China. Electronic address: .

Abstract:  This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal. 

Retracted: No

PubPeer comments:
 This paper has been withdrawn. The paper itself has disappeared and was replaced by the following message:  *This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https: www.elsevier.com about our-business policies article-withdrawal.* It is unfortunate that publisher Elsevier does not follow COPE guidelines, by removing the paper instead of e.g. watermarking it with a retraction sign. ,