PReD-Bench/PRed-Bench huggingface dataset:
Retraction: α‐GalCer ameliorates listeriosis by accelerating infiltration of Gr‐1 +  cells into the liver
Authors: Volker Brinkmann
Robert Hurwitz
Yoshiko Emoto
Takamitsu Shimizu
M Emoto
Izumi Yoshizawa
Eiji Kita
Stefan H. E Kaufmann
Journal: European Journal of Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: Retraction; Emoto; Listeriosis; Gr-1+ cells; Liver

Abstract:  Retraction: Emoto, M., Emoto, Y., Yoshizawa, I., Kita, E., Shimizu, T., Hurwitz, R., Brinkmann, V. and Kaufmann, S.H.E. (2010), α-GalCer ameliorates listeriosis by accelerating infiltration of Gr-1+ cells into the liver. Eur. J. Immunol., 40: 1328-1341. DOI: https://doi.org/10.1002/eji.200939594 The above article, published online on 16 February 2010 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the Chairman of the Executive Committee of the European Journal of Immunology and Wiley-VCH Verlag GmbH &amp; Co. KGaA. The retraction has been agreed following an investigation carried out by Gunma University (http://www.gunma-u.ac.jp/wp-content/uploads/2017/10/chosakekka29.pdf). The investigation was unable to determine the validity of the images for which Professor Emoto, the article's corresponding author, was responsible. As a result, the journal has made the decision to retract the article. 

Retracted: No

PubPeer comments:
 Abstract Retraction: Emoto, M., Emoto, Y., Yoshizawa, I., Kita, E., Shimizu, T., Hurwitz, R., Brinkmann, V. and Kaufmann, S.H.E. (2010), u03b1u2010GalCer ameliorates listeriosis by accelerating infiltration of Gru20101+ cells into the liver. Eur. J. Immunol., 40: 1328u20131341. DOI: https: doi.org 10.1002 eji.200939594 The above article, published online on 16 February 2010 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the Chairman of the Executive Committee of the European Journal of Immunology and Wileyu2010VCH Verlag GmbH Co. KGaA. The retraction has been agreed following an investigation carried out by Gunma University (http: www.gunma-u.ac.jp wp-content uploads 2017 10 chosakekka29.pdf). The investigation was unable to determine the validity of the images for which Professor Emoto, the article s corresponding author, was responsible. As a result, the journal has made the decision to retract the article. ,
Knockdown of LncRNA ANRIL suppresses cell proliferation, metastasis, and invasion via regulating miR-122-5p expression in hepatocellular carcinoma
Authors: Huifeng Yuan
Tengfei Li
Ji Ma
Xinwei Han
Journal: Journal of Cancer Research and Clinical Oncology (2018)
Discipline: CLINICAL MEDICINE
Keywords: ANRIL; HCC; Invasion; Metastasis; MiR-122-5p
Affiliations: Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China., Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China. .

Abstract:  Objective: Previous studies reported that lncRNA antisense non-coding RNA in the INK4 locus (ANRIL) was upregulated in hepatocellular carcinoma (HCC) tissues and decreased expression of ANRIL could suppress cell proliferation, metastasis, and invasion and induce apoptosis of HCC cells. However, the molecular mechanism of ANRIL involved in HCC tumorigenesis is still unknown. Methods: The expressions of ANRIL and miR-122-5p in HCC tissues and cells were quantified by qRT-PCR. MTT assay, colony formation assay, wound healing assay, and transwell invasion assay were performed to evaluate cell growth, metastasis, and invasion, respectively. RNA immunoprecipitation (RIP) assay and luciferase reporter assay were performed to determine whether ANRIL could directly bind to miR-122-5p in HCC cells. Xenograft tumor experiment was conducted to confirm the biological role and underlying mechanism of ANRIL in vivo. Results: The results showed that ANRIL was upregulated and miR-122-5p was downregulated in HCC tissues and cells. ANRIL was negatively correlated with miR-122-5p expression in HCC tissues. Knockdown of ANRIL or miR-122-5p overexpression suppressed HCC cell viability, colony formation ability, metastasis, and invasion. ANRIL was demonstrated to directly bind to miR-122-5p and inhibit its expression. Forced expression of ANRIL abolished the inhibitory effect of miR-122-5p overexpression on HCC progression. In vivo experiment demonstrated that ANRIL knockdown impeded tumor growth in vivo and increased miR-122-5p expression. Conclusion: Our finding suggested that knockdown of ANRIL suppressed cell proliferation, metastasis and invasion via regulating miR-122-5p expression in HCC, illustrating the underlying mechanism of the oncogenic role of ANRIL in HCC. 

Retracted: No

PubPeer comments:
  Fig. 1 Expression levels of ANRIL and miR-122-5p in HCC tissues. qRT-PCR analysis was conducted to assess the expression levels of ANRIL (a) and miR-122-5p (b) in 31 paired HCC tissues and their corresponding adjacent normal tissues. c Negative correlation between ANRIL and miR-122-5p expression . The swarm plots for HCC expression of (a) ANRIL and (b) miR-122-5p should simply be the marginal distributions of the horizontal and vertical axes respectively of scatterplot in (c) -- each point in (c) should have corresponding points in both swarms with the same horizontal- or vertical-axis values. In fact I can see no clear relationship. ![file] ,
Viral Capsids Mimicking Based on pH-Sensitive Biodegradable Polymeric Micelles for Efficient Anticancer Drug Delivery
Authors: Qingqing Huo
Jie Cao
Yuji Pu
Wei Lu
Yan Liang
Bin He
Lutao Jiang
Shangcong Han
Yong Sun
Journal: Journal of Biomedical Nanotechnology (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bio-inspired; supramolecular self-assembly; drug delivery; viral capsid analogue; pH-Sensitive

Abstract:  Bio-inspired supramolecular self-assembly have been widely explored in biomedical engineering, especially in the field of drug delivery. Here, viral capsid analogue pH-Sensitive polymeric micelles HA-Hyd-DOX were reported, where natural polysacarrides hyaluronic acid (HA) and anticancer drug doxorubicin (DOX), were linked through a hydrazone bond with a high drug loading content of 33.09 wt%. The polymeric micelles look like artificial virus capsids from "core-shell" structures. In addition, the polymeric backbone HA and hydrazone bonds were destroyed in the presence of hyaluronidase in cancer cells and under the acidic conditions of pH = 5 respectively, thereby prodrug-based polymeric micelles could penetrate into the tumor and DOX could be released in lysosomes to enhance anticancer efficacy. With the comparison of typical prodrug-based polymeric micelles mPEG-Hyd-DOX system where DOX was linked to methoxy poly(ethylene glycol) with a hydrazone bond linkage, HA-Hyd-DOX showed greater inhibition to cancer cells due to the better penetration. Such viral capsids mimicking polymeric micelles provided some remarkable benefits for drug delivery, including, high drug loading efficiency, controlled drug release and excellent biodegradable. 

Retracted: No

PubPeer comments:
 Confocal images in the red frame in Figure 6 are the same one!![file] , 
 #1 Thank you very much for pointing out our naive error. We are very sorry for our lack of rigor and have not found such an obvious low-level error. After checking the original data and the people who participated in the experiment, the two lines of image in the article are the same but the light intensity is different, which was groping for lighting conditions for the confocal laser scanning microscopy experiment. But at that time, the test picture was named 1-1 and our corresponding experimental group picture was named 1. And we are terribly sorry that during processing the images, we made a such a low-level mistake. The corresponding experimental group should be this image: ![file] we have contacted the editor of Journal of Biomedical Nanotechnology to correct the mistake. In addition, we deeply apologize for our terrible carelessness, and we are grateful for your reminding. We attach all the original data corresponding to the above: ![file] ![file] , 
 #2 ![file] ![file] ![file] ![file] , 
 #1 Our errata has been completed online on October 20, 2020. ,
Gastroprotective activity of polyphenolic-rich extract of Potentilla mooniana
Authors: S Hemalatha
Krishnamurthy Sairam
Satyendra K Prasad
Damiki Laloo
Journal: Pharmaceutical Biology (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Antioxidant; ethanol; gastric-ulcer; histopathology; mucus
Affiliations: Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University) , Varanasi, Uttar Pradesh , India.

Abstract:  Context: Potentilla mooniana Wight. (Rosaceae) is a plant found in the Himalayan region where the root is traditionally used to treat stomach problems including gastric-ulcer. Objective: To scientifically validate the gastro-protective effect and derive the possible mechanistic activity of the ethanol root extract from P. mooniana (EPM). Materials and methods: The gastroprotective effect of EPM (100-400 mg/kg, p.o.) was evaluated on both the physical (Pyloric ligation, PL; Cold restrain stress, CRS) and chemical (absolute ethanol, EtOH; aspirin, ASP) ulcerogens induced ulceration in rats. The mechanistic activity of EPM was tested on various gastric-ulcer parameters, namely gastric pH, volume, acid-pepsin output, DNA content, histamine level, H(+)K(+)-ATPase activity, mucus content, microvascular permeability, antioxidant markers, and gastric-histopathological study. Results: EPM significantly reduces the ulcer score against all the four tested gastric-ulcer models. In the PL model, EPM showed significant reduction (p &lt; 0.05) in acid-pepsin output and cell shedding; however, no significant effect was observed on gastric volume, cell proliferation, stomach glandular weight, and histamine levels. EPM (400 mg/kg, p.o.) when compared with ulcer control showed significant increase in gastric pH by 41.6% and decrease in H(+)K(+)-ATPase activity by 47.73%. In addition, EPM showed significant increase in mucus content by 58.60% and a decrease in the microvascular permeability of Evans Blue by 85.00%, justifying its protective effects. Furthermore, EPM also showed significant antioxidant activity and histopathologically possessed excellent cytoprotective effect. Conclusion: The gastro-protective effect of EPM is attributed mainly to the defensive mechanism owing to the presence of a good quantity of polyphenolic components. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: Panel  Group II (Ulcer control) looks similar to panel E1 in Figure 4 from an older paper by the same authors. That older paper is Damiki Laloo et al., Journal of Ethnopharmacology 146 (2013) 505u2013514, DOI: 10.1016 j.jep.2013.01.015. In Laloo 2013, panel E1 = EPF (P. fulgens ethanolic root extract) pre-treated rats. Could the authors please clarify if these two panels represent the exact same treatment? ![file] ,
Mitochondrial Localization and Function of Heme Oxygenase-1 in Cigarette Smoke–Induced Cell Death
Authors: Fang Liu
Fengli Guo
Hong Pyo Kim
Augustine M K Choi
Jenny M Karlsson
Marco van der Toorn
Simon C Watkins
Henk F Kauffman
Dirk-Jan Slebos
Dirkje S Postma
Janet S Lee
Catherine J Baty
Xue Wang
Stefan W Ryter
Journal: American journal of respiratory cell and molecular biology (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cigarette smoke; apoptosis; necrosis; chronic obstructive pulmonary disease; heme oxygenase-1
Affiliations: Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, MUH 628NW, 3459 Fifth Ave., Pittsburgh, PA 15213, USA.

Abstract:  Cigarette smoke-induced apoptosis and necrosis contribute to the pathogenesis of chronic obstructive pulmonary disease. The induction of heme oxygenase-1 provides cytoprotection against oxidative stress, and may protect in smoking-related disease. Since mitochondria regulate cellular death, we examined the functional expression and mitochondrial localization of heme oxygenase-1 in pulmonary epithelial cells exposed to cigarette smoke extract (CSE), and its role in modulating cell death. Heme oxygenase-1 expression increased dramatically in cytosolic and mitochondrial fractions of human alveolar (A549), or bronchial epithelial cells (Beas-2b) exposed to either hemin, lipopolysaccharide, or CSE. Mitochondrial localization of heme oxygenase-1 was also observed in a primary culture of human small airway epithelial cells. Furthermore, heme oxygenase activity increased dramatically in mitochondrial fractions, and in whole cell extracts of Beas-2b after exposure to hemin and CSE. The mitochondrial localization of heme oxygenase-1 in Beas-2b was confirmed using immunogold-electron microscopy and immunofluorescence labeling on confocal laser microscopy. CSE caused loss of cellular ATP and rapid depolarization of mitochondrial membrane potential. Apoptosis occurred in Beas-2b at low concentrations of cigarette smoke extract, whereas necrosis occurred at high concentrations. Overexpression of heme oxygenase-1 inhibited CSE-induced Beas-2b cell death and preserved cellular ATP levels. Finally, heme oxygenase-1 mRNA expression was elevated in the lungs of mice chronically exposed to cigarette smoke. We demonstrate the functional compartmentalization of heme oxygenase-1 in the mitochondria of lung epithelial cells, and its potential role in defense against mitochondria-mediated cell death during CSE exposure. 

Retracted: No

PubPeer comments:
 Figure 1D this paper. Much more similar than expected after vertical re-sizing. https: imgur.com BVywkLb ,
Simultaneous over-expression of PaSOD and RaAPX in transgenic Arabidopsis thaliana confers cold stress tolerance through increase in vascular lignifications
Authors: Paramvir Singh Ahuja
Yelam Sreenivasulu
Tejpal Gill
Amrina Shafi
Vivek Dogra
Journal: PloS one (2014)
Discipline: Multidisciplinary
Keywords: Antioxidant enzymes; cold stress tolerance; transgenic plants; reactive oxygen species; gene expression
Affiliations: Division of Biotechnology, CSIR-Institute of Himalayan Bioresource Technology, Palampur, Himachal Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), CSIR- Institute of Himalayan Bioresource Technology, Palampur, Himachal Pradesh, India., Division of Biotechnology, CSIR-Institute of Himalayan Bioresource Technology, Palampur, Himachal Pradesh, India.

Abstract:  Antioxidant enzymes play a significant role in eliminating toxic levels of reactive oxygen species (ROS), generated during stress from living cells. In the present study, two different antioxidant enzymes namely copper-zinc superoxide dismutase derived from Potentilla astrisanguinea (PaSOD) and ascorbate peroxidase (RaAPX) from Rheum austral both of which are high altitude cold niche area plants of Himalaya were cloned and simultaneously over-expressed in Arabidopsis thaliana to alleviate cold stress. It was found that the transgenic plants over-expressing both the genes were more tolerant to cold stress than either of the single gene expressing transgenic plants during growth and development. In both single (PaSOD, RaAPX) and double (PaSOD + RaAPX) transgenic plants higher levels of total antioxidant enzyme activities, chlorophyll content, total soluble sugars, proline content and lower levels of ROS, ion leakage were recorded when compared to the WT during cold stress (4°C), besides increase in yield. In the present study, Confocal and SEM analysis in conjunction with qPCR data on the expression pattern of lignin biosynthetic pathway genes revealed that the cold stress tolerance of the transgenic plants might be because of the peroxide induced up-regulation of lignin by antioxidant genes mediated triggering. 

Retracted: No

PubPeer comments:
 ![file] ,
The Not5 subunit of the ccr4-not complex connects transcription and translation
Authors: Olesya O Panasenko
Ishaan Gupta
Sari Kassem
Imre Boros
Zoltan Villanyi
Lars Steinmetz
Virginie Ribaud
Zoltan Pahi
Martine A Collart
Journal: PLoS genetics (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RNA polymerase II; Rpb4; Rpb7; gene expression; Ccr4-Not complex
Affiliations: Department of Microbiology and Molecular Medicine, University of Geneva, Faculty of Medicine, Geneva, Switzerland; Institute of Genetics and Genomics of Geneva, Geneva, Switzerland., Department of Biochemistry and Molecular Biology, University of Szeged, Szeged, Hungary., European Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg, Germany.

Abstract:  Recent studies have suggested that a sub-complex of RNA polymerase II composed of Rpb4 and Rpb7 couples the nuclear and cytoplasmic stages of gene expression by associating with newly made mRNAs in the nucleus, and contributing to their translation and degradation in the cytoplasm. Here we show by yeast two hybrid and co-immunoprecipitation experiments, followed by ribosome fractionation and fluorescent microscopy, that a subunit of the Ccr4-Not complex, Not5, is essential in the nucleus for the cytoplasmic functions of Rpb4. Not5 interacts with Rpb4; it is required for the presence of Rpb4 in polysomes, for interaction of Rpb4 with the translation initiation factor eIF3 and for association of Rpb4 with mRNAs. We find that Rpb7 presence in the cytoplasm and polysomes is much less significant than that of Rpb4, and that it does not depend upon Not5. Hence Not5-dependence unlinks the cytoplasmic functions of Rpb4 and Rpb7. We additionally determine with RNA immunoprecipitation and native gel analysis that Not5 is needed in the cytoplasm for the co-translational assembly of RNA polymerase II. This stems from the importance of Not5 for the association of the R2TP Hsp90 co-chaperone with polysomes translating RPB1 mRNA to protect newly synthesized Rpb1 from aggregation. Hence taken together our results show that Not5 interconnects translation and transcription. 

Retracted: No

PubPeer comments:
 Figure 3A: * Red boxes: In the top left CHX not5delta panel, lanes 13 and 14 look similar to lanes 15 and 16. ![file] , 
 Figure 5C. * Aqua blue boxes: The WT Rpb1 panel looks similar to the not5delta Rpb1 panel, although at a different zoom and exposure level. Note the presence of a little slanted stripe to the right of the fattest band in lanes 1. ![file] ,
Antiviral activities of atractylon from Atractylodis Rhizoma
Authors: Tian-Lu Hou
Yang Cheng
Jian Ping
Jing-Yin Mai
Jian-Jie Chen
Journal: Molecular Medicine Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: Atractylodis Rhizoma; antiviral activities; atractylon; influenza A virus; pulmonary injury
Affiliations: Department of Infectious Disease, Hospital for Infectious Diseases of Pudong New Area, Shanghai 201299, P.R. China., Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.

Abstract:  Atractylodis Rhizoma is a traditional medicinal herb, which has antibacterial, antiviral, anti‑inflammatory and anti‑allergic, anticancer, gastroprotective and neuroprotective activities. It is widely used for treating fever, cold, phlegm, edema and arthralgia syndrome in South‑East Asian nations. In this study, 6 chemical compositions of Atractylodis Rhizoma were characterized by spectral analysis and their antiviral activities were evaluated in vitro and in vivo. Among them, atractylon showed most significant antiviral activities. Atractylon treatment at doses of 10‑40 mg/kg for 5 days attenuated influenza A virus (IAV)‑induced pulmonary injury and decreased the serum levels of interleukin (IL)‑6, tumor necrosis factor‑α and IL‑1β, but increased interferon‑β (IFN‑β) levels. Atractylon treatment upregulated the expression of Τoll‑like receptor 7 (TLR7), MyD88, tumor necrosis factor receptor‑associated factor 6 and IFN‑β mRNA but downregulated nuclear factor‑κB p65 protein expression in the lung tissues of IAV‑infected mice. These results demonstrated that atractylon significantly alleviated IAV‑induced lung injury via regulating the TLR7 signaling pathway, and may warrant further evaluation as a possible agent for IAV treatment. 

Retracted: No

PubPeer comments:
 Would the authors be able to post the original scans for figure 3B? At the current resolution, it appears several bands have been repeated, and a higher resolution image or original scans might address this concern. *** False color ![file] *** Original ![file] ,
Chinese medicine Di-Huang-Yi-Zhi protects PC12 cells from H2O2-induced apoptosis by regulating ROS-ASK1-JNK/p38 MAPK signaling
Authors: Hong-Mei An
Miao Jin
Rong-Rong Zhen
Bing Hu
Li-Min Zhang
Tian-Li Zhang
Chao Gu
Yue Li
Journal: BMC Complementary Medicine and Therapies (2020)
Discipline: CLINICAL MEDICINE
Keywords: Alzheimer’s disease; Apoptosis; Chinese herb; Di-Huang-Yi-Zhi; Oxidative stress
Affiliations: Department of Neurology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China., Department of Oncology, Institute of Traditional Chinese Medicine in Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. ., Department of Science & Technology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. .

Abstract:  Background: Oxidative stress mediates the nerve injury during the pathogenesis of Alzheimer's disease (AD). Protecting against oxidative stress damage is an important strategy to prevent and treat AD. Di-Huang-Yi-Zhi (DHYZ) is a Chinese medicine used for the treatment of AD, but its mechanism remains unknown. This study is aimed to investigate the effect of DHYZ on H2O2 induced oxidative damage in PC12 cells. Methods: PC12 cells were treated with H2O2 and DHYZ. Cell proliferation was detected by Cell counting kit-8 (CCK-8) assay. Cytotoxicity of H2O2 was measured by lactate dehydrogenase (LDH) release assay. Apoptosis were identified by Annexin V-FITC/PI staining. Caspase 3 activity was detected by commercial kit. Mitochondrial membrane potential (MMP) was detected by JC-1 staining. Reactive oxygen species (ROS) was 2', 7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) staining. Protein expression and phosphorylation was identified by western blot. Results: The results showed that DHYZ antagonized H2O2-mediated cytotoxicity and proliferation inhibition. DHYZ reduced ROS production, stabilize mitochondrial membrane potential, inhibit Caspase-3 activity and apoptosis induced by H2O2. In addition, DHYZ inhibited the phosphorylation of ASK1, JNK1/2/3 and p38 MAPK which were up-regulated by H2O2. Conclusions: The present study suggested that DHYZ protected PC12 cells from H2O2-induced oxidative stress damage and was related to inhibition of ROS production and ASK1-JNK/p38 MAPK signaling. The present study provides experimental evidence for the application of DHYZ for the management of oxidative stress damage and AD. 

Retracted: Yes

PubPeer comments:
 The actin for astrocytes and C6 in panel c) and d) looks identical ![file] ![file] ,
MicroRNA-337 regulates the PI3K/AKT and Wnt/β-catenin signaling pathways to inhibit hepatocellular carcinoma progression by targeting high-mobility group AT-hook 2
Authors: Ruijin Song
Hongzhang Cui
Xi Chen
Jiajun Yin
Ju Wu
Wei Wang
Journal: American journal of cancer research (2018)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocellular carcinoma; high-mobility group AT-hook 2; microRNA-337; tumor suppressor.
Affiliations: Department of Hepatobiliary and Pancreatic Laparoscopic Surgery, Affiliated Zhongshan Hospital of Dalian UniversityDalian 116300, Liaoning, China., Department of Interventional, Sixth People's Hospital of DalianDalian, Liaoning, China.

Abstract:  MicroRNAs (miRNAs) serve as major regulators during the tumorigenesis and tumor development of hepatocellular carcinoma (HCC). In addition, miRNAs may serve as new promising biomarkers for the diagnosis and prognosis and as effective therapeutic targets for patients with this malignancy. Therefore, understanding the association between miRNAs and HCC may be beneficial to discover novel therapeutic approaches towards diagnosis and treatments. Results of this study showed that miRNA-337 (miR-337) was markedly downregulated in HCC tissues and cell lines. Decreased miR-337 expression was significantly associated with the TNM stage and lymph node metastasis of HCC. Ectopic expression of miR-337 prohibited the proliferation, colony formation, migration, and invasion of HCC cells. It also promoted the apoptosis in vitro and reduced the tumor growth in vivo of these cells. High-mobility group AT-hook 2 (HMGA2) was identified as a direct target gene of miR-337 in HCC through a series of experiments. HMGA2 was significantly overexpressed in HCC tissues and negatively correlated with miR-337 expression. Moreover, the functions of HMGA2 inhibition were similar to those induced by miR-337 in HCC. Restored HMGA2 expression rescued the tumor-suppressive roles of miR-337 overexpression in HCC. Furthermore, miR-337 overexpression inhibited the activation of PI3K/AKT and Wnt/β-catenin signaling pathways in HCC both in vitro and in vivo. This study demonstrated that miR-337 may play tumor-suppressing roles in HCC, at least partly, via directly targeting HMGA2 and inhibiting the PI3K/AKT and Wnt/β-catenin signaling pathways. Therefore, miR-337 may be a novel and effective target for the therapeutic treatment of patients with HCC. 

Retracted: No

PubPeer comments:
 Figs 2D, 6F, 7F. ![file] Two panels appear to be the same (pink boxes). Blue box marks a panel that also appears in Figs 2C, 4C, 5D of [Lyu et al (2019)] . ![file] ![file] There may be matches with other panels, or with other papers in this oeuvre. https: docs.google.com spreadsheets d 1X401JM6CcpTSkbKsPsOl20pRKQ-ns1S_J5pTwtBjqPw edit#gid=0 ,
Changes in innate and permissive immune responses after hbv transgenic mouse vaccination and long-term-siRNA treatment [corrected]
Authors: Hong-Bin Zhang
Guang-Yu Huang
Wei-Yun Zhang
Ying Fang
Guang-Li Ren
Jian Liu
Hong Zheng
Wen-Kui Hu
Heng-Hao Ma
Da-Yong Sun
Man-Chun Xu
Ya-Gang Zhao
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: HBV; siRNA; immune response; transgenic mice; vaccination
Affiliations: Department of Pediatrics, General Hospital of GuangZhou Military Command of PLA, GuangZhou, China. 

Abstract:  Background: Currently, no licensed therapy can thoroughly eradicate hepatitis B virus (HBV) from the body, including interferon α and inhibitors of HBV reverse-transcription. Small interfering RNA (siRNA) seem to be a promising tool for treating HBV, but had no effect on the pre-existing HBV covalently closed circular DNA. Because it is very difficult to thoroughly eradicate HBV with unique siRNAs, upgrading the immune response is the best method for fighting HBV infection. Here, we aim to explore the immune response of transgenic mice to HBV vaccination after long-term treatment with siRNAs and develop a therapeutic approach that combines siRNAs with immunopotentiators. Methodology/principal findings: To explore the response of transgenic mice to hepatitis B vaccine, innate and acquired immunity were detected after long-term treatment with siRNAs and vaccination. Antiviral cytokines and level of anti-hepatitis B surface antigen antibody (HBsAg-Ab) were measured after three injections of hepatitis B vaccine. Results: Functional analyses indicated that toll-like receptor-mediated innate immune responses were reinforced, and antiviral cytokines were significantly increased, especially in the pSilencer4.1/HBV groups. Analysis of CD80+/CD86+ dendritic cells in the mouse liver indicated that dendritic cell antigen presentation was strengthened. Furthermore, the siRNA-treated transgenic mice could produce detectable HBsAg-Ab after vaccination, especially in the CpG oligonucleotide vaccine group. Conclusions/significance: For the first time, our studies demonstrate that siRNAs with CpG HBV vaccine could strengthen the immune response and break the immune tolerance status of transgenic mice to HBV. Thus, siRNAs and HBV vaccine could provide a sharp double-edged sword against chronic HBV infection. 

Retracted: No

PubPeer comments:
 Fig 2.  Colony growth (H) in Caki-1 cells transfected with mimic ctrl or miR-337-3p mimic and (I) in 786-O cells transfected with inhibitor ctrl or miR-337-3p inhibitor was determined by colony formation assay. ![file] Two cookies are cut from the same dough, albeit with a 75-deg rotation. ,
The role of gut microbiota in the pathogenesis and management of allergic diseases
Authors: D Compare
G Nardone
Journal: European review for medical and pharmacological sciences (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Allergy; Hypersensitivity reaction; Immunologic mechanisms; Epidemiological studies; Allergic disorders
Affiliations: Department of Clinical Medicine and Surgery, Gastroenterology Unit, Federico II University of Naples, Italy. .

Abstract:  Allergy is defined as a hypersensitivity reaction due to specific antibody-mediated or cell-mediated immunologic mechanisms. Epidemiological studies are showing a dramatic increase of allergies in industrialized countries in the last few decades, while remaining stable in developing countries. In 1989 Strachan, hypothesized that the increase in allergic disorders was the result of a lack of infections in early infancy, and in 1998 Wold suggested that, rather than a decrease in viral or bacterial infections, an altered normal intestinal colonization pattern in infancy, could be responsible for the increase in allergies. Germ-free mice were shown to mount an exaggerated allergic airway reaction compared with that seen in colonized mice, indicating the important role of microbe-host interactions in the development of allergic diseases. Infants with food allergies are found to exhibit an imbalance between "beneficial"and potentially harmful bacteria, i.e., decreased Lactobacilli, Bifidobacteria and Enterococcus species and increased coliforms, Staphylococcus aureus and Clostridium species, suggesting that microbial inhabitants of the human body, may play either a pathogenic or protective role in allergies. Based on this data, many clinical trial addressing the use of probiotics in the context of allergic disorders, have been conducted in children. However, currently, no conclusive item may be drawn. 

Retracted: No

PubPeer comments:
 This article has been retracted some time in 2014. Although the retraction notice just says the article was withdrawn, it was because of plagiarism, reported in January 2014. Here is an overview of the text of the paper, with highlights in different colors showing verbatim textual similarities to 11 older papers by other authors. Nine of these were listed in the References, but the text was not between quotes. ![file] Here is a detailed view of the key to the color coding of the source documents. ![file] ,
Age-related changes of protein SUMOylation balance in the AÎ²PP Tg2576 mouse model of Alzheimer's disease
Authors: Lucia Negri
Jan Egebjerg
Robert Nisticò
Fabio Blandini
Veronica Marconi
Caterina Ferraina
Marco Feligioni
Journal: Frontiers in Pharmacology (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Alzheimer's disease; SENP1; SUMO-1; SUMO-2/3; Tg2576
Affiliations: IRCCS Fondazione Santa Lucia Rome, Italy ; Department of Physiology and Pharmacology, Sapienza University of Rome Rome, Italy., Laboratory of Pharmacology of Synaptic Plasticity, EBRI "Rita Levi-Montalcini" Foundation Rome, Italy., Department of Physiology and Pharmacology, Sapienza University of Rome Rome, Italy., Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute Pavia, Italy., Neuroscience Drug Discovery DK H. Lundbeck A/S, Valby, Denmark.

Abstract:  Alzheimer's disease (AD) is a complex disorder that affects the central nervous system causing a severe neurodegeneration. This pathology affects an increasing number of people worldwide due to the overall aging of the human population. In recent years SUMO protein modification has emerged as a possible cellular mechanism involved in AD. Some of the proteins engaged in the physiopathological process of AD, like BACE1, GSK3-β tau, AβPP, and JNK, are in fact subject to protein SUMO modifications or interactions. Here, we have investigated the SUMO/deSUMOylation balance and SUMO-related proteins during the onset and progression of the pathology in the Tg2576 mouse model of AD. We examined four age-stages (1.5, 3, 6, 17 months old) and observed shows an increase in SUMO-1 protein conjugation at 3 and 6 months in transgenic mice with respect to WT in both cortex and hippocampus. Interestingly this is paralleled by increased expression levels of Ubc9 and SENP1 in both brain regions. At 6 months of age also the SUMO-1 mRNA resulted augmented. SUMO-2-ylation was surprisingly decreased in old transgenic mice and was unaltered in the other time windows. The fact that alterations in SUMO/deSUMOylation equilibrium occur from the early phases of AD suggests that global posttranslational modifications may play an important role in the mechanisms underlying disease pathogenesis, thus providing potential targets for pharmacological interventions. 

Retracted: No

PubPeer comments:
 The same actin bands in Fig. 1A and B: ![file] The same beta-actin bands were used in Fig. 2A and C: ![file] ,
Overexpressing TGF-β1 in mesenchymal stem cells attenuates organ dysfunction during CLP-induced septic mice by reducing macrophage-driven inflammation
Authors: Shi Zhang
Jianfeng Xie
Xiwen Zhang
Ming Xue
Zongsheng Wu
Haibo Qiu
Yi Yang
Jianxiao Chen
Feng Liu
Journal: Stem Cell Research & Therapy (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Macrophage activation; Mesenchymal stem cells; Sepsis; Transforming growth factor-β1.
Affiliations: Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, 210009, China., Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, 210009, China. .

Abstract:  Background: Sepsis remains a leading cause of death in critically ill patients. It is well known that mesenchymal stem cells (MSCs) are a promising therapy partly due to their paracrine-mediated immunoregulatory function. Previous study demonstrated that transforming growth factor-beta1 (TGF-β1) is an important cytokine secreted by MSCs and that it participates in MSC-mediated macrophage phenotype switch from pro-inflammatory to pro-resolution. In addition, the transformation of macrophage phenotype may be a potential treatment for sepsis. However, the therapeutic effect of overexpressing TGF-β1 in MSCs (MSC-TGF-β1) on sepsis is not well understood. Therefore, this study aimed to evaluate the effects of TGF-β1 overexpressing MSCs on organ injury in cecal ligation and puncture (CLP)-induced septic mice and to detect the changes in macrophage phenotype during this process. Methods: Mouse MSCs stably transfected with TGF-β1 were constructed and injected into CLP-induced septic mice via tail vein. After 24 h, the mice were sacrificed; then, the histopathology of the organ was evaluated by hematoxylin-eosin (H&amp;E) staining. Inflammatory cytokines were detected by ELISA. Macrophage infiltration and phenotype transformation in the tissues were determined by immunohistochemistry and flow cytometry. In addition, we performed adoptive transfer of mouse peritoneal macrophage pretreated with TGF-β1 overexpressing MSCs in septic mice. Results: We found that infusion of TGF-β1 overexpressing MSCs attenuated the histopathological impairment of the organ, decreased the pro-inflammatory cytokine levels and inhibited macrophage infiltration in tissues. TGF-β1 overexpressing MSCs induced macrophage phenotypes changed from pro-inflammatory to pro-resolution in inflammatory environment. The adoptive transfer of mouse peritoneal macrophages pretreated with TGF-β1 overexpressing MSCs also relieved organ damage in CLP-induced septic mice. Conclusion: Under septic conditions, TGF-β1 overexpressing MSCs can enhance the therapeutic effects of MSCs on organ injury and inflammation as a result of reduced macrophage infiltration and induced macrophages transformation, the adoptive transfer of macrophages treated with TGF-β1 overexpressing MSCs also relieved organ damage. This will provide new hope for the treatment of sepsis. 

Retracted: No

PubPeer comments:
 Figure 3F appears to have two images which overlap (red boxes). *** ![file] ![file] ,
LncRNA MAGI2-AS3 suppresses the proliferation and invasion of non-small cell lung carcinoma through miRNA-23a-3p/PTEN axis
Authors: X-Z Hao
K Yang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA MAGI2-AS3; non-small cell lung carcinoma (NSCLC); biological role; molecular mechanism; tumor size
Affiliations: Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, .

Abstract:  Objective: To uncover the biological role of long non-coding RNA (lncRNA) MAGI2-AS3 in the progression of non-small cell lung carcinoma (NSCLC) and its molecular mechanism. Patients and methods: LncRNA MAGI2-AS3 level in NSCLC tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Chi-square test was conducted to analyze the correlation between MAGI2-AS3 level and pathological characteristics of NSCLC patients. Survival analysis was performed in NSCLC patients with high expression or low expression of MAGI2-AS3. In vitro influences of MAGI2-AS3 on viability and invasive ability of A549 and PC9 cells were evaluated. MicroRNA-23a-3p (miRNA-23a-3p), the target gene of MAGI2-AS3 was determined through the dual-luciferase reporter gene assay. In a similar way, the target gene of miRNA-23a-3p was identified. Finally, the regulatory effect of MAGI2-AS3/miRNA-23a-3p/PTEN (gene of phosphate and tension homology deleted on chromosome ten) axis on cellular behaviors of NSCLC cells was assessed. Results: LncRNA MAGI2-AS3 was downregulated in NSCLC tissues and cell lines. Its level was closely related to tumor size, Tumor Node Metastasis (TNM) stage and distant metastasis of NSCLC patients. The worse prognosis was identified in NSCLC patients with low expression of MAGI2-AS3 relative to those with a high expression. Overexpression of MAGI2-AS3 markedly attenuated viability and invasive ability of A549 and PC9 cells. MiRNA-23a-3p was verified to be the target gene of MAGI2-AS3, and furthermore, PTEN was the target of miRNA-23a-3p. Overexpression of miRNA-23a-3p could reverse the inhibited viability and invasion in NSCLC cells overexpressing MAGI2-AS3. Conclusions: MAGI2-AS3 is downregulated in NSCLC. Overexpression of MAGI2-AS3 suppresses the proliferative and invasive abilities of NSCLC via miRNA-23a-3p/PTEN axis. 

Retracted: No

PubPeer comments:
 From the methods:  40 paired tumor tissues and matched adjacent tissues were surgically resected from NSCLC patients treated in Beijing Chaoyang District Sanhuan Cancer Hospital from December 2016 to March 2018. The paper was published in September 2019. Yet, Figure 1D shows that the patients were followed for four years (around 48 months). Can the authors explain how they were able to do this? ![file] ,
RETRACTED: Autoimmunity as a Consequence of Retrovirus-Mediated Expression of C-FLIP in Lymphocytes
Authors: Y Refaeli
A K Abbas
D Baltimore
L Van Parijs
Journal: Immunity (1999)
Discipline: IMMUNOLOGY
Keywords: apoptosis; death receptors; FLICE inhibitory proteins (FLIPs); lymphocytes; c-FLIP

Abstract:  The induction of apoptosis by death receptors serves to regulate immune responses by eliminating unwanted and harmful cells. Mature lymphocytes express FLICE inhibitory proteins (FLIPs) that block death receptor-induced cell death. Here, we show that both B and T cells downregulate c-FLIP upon activation in vitro. Retrovirus-mediated expression of c-FLIP blocks Fas-induced apoptosis of activated lymphocytes but does not affect cell death resulting from cytokine withdrawal. In vivo, c-FLIP expression results in defective superantigen-mediated elimination of T cells, the accumulation of activated B cells, the production of autoantibodies, and the development of autoimmune disease. No effect was seen on negative selection of thyomocytes. These results suggest that activation-dependent downregulation of c-FLIP renders mature lymphocytes sensitive to death receptor-mediated apoptosis and is required to maintain self-tolerance. 

Retracted: No

PubPeer comments:
 2009 retraction https: www.cell.com immunity fulltext S1074-7613(09)00154-X?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS107476130900154X%3Fshowall%3Dtrue The authors have agreed to retract this paper because of duplication of the flow cytometry dot plots in Figure 5 [labeled as u201cInfected (GFP+)u201d and u201cNot infected (GFPu2212)u201d; lower panels] by the first author. This figure shows the IgM expression on B cells from mice with and without FLIP expression. These panels are important for showing that cells not expressing FLIP are not affected by the FLIP-expressing cells in the same mice. This matter was investigated by the California Institute of Technology and the Office of Research Integrity at the United States Department of Human Services, which found the first author to be responsible for the scientific misconduct pertaining to the issue described here. The authors stand by the validity of the other figures and sincerely apologize for the inconvenience caused by this retraction. ,
Aberrant regulation of survivin by the RB/E2F family of proteins
Authors: Rachel A Altura
Yuying Jiang
Michael P Holloway
Gustavo Leone
Harold I Saavedra
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Survivin; oncogene; cancer cells; transcriptional processes; genes
Affiliations: Columbus Children's Research Institute, College of Medicine and Public Health, Ohio State University, 43210, USA.

Abstract:  Survivin is a putative oncogene that is aberrantly expressed in cancer cells. It has been hypothesized to play a central role in cancer progression and resistance to therapy in diverse tumor types. Although some of the transcriptional processes regulating its expression have been established, the diversity of genes that may be controlling the levels of its expression in both normal cells as well as in cancer cells has not been fully explored. The most common genetically mutated pathways in human malignancies are the p53 tumor suppressor pathway and the RB/E2F pathway. Both of these pathways, when intact, provide essential checkpoints in the maintenance of normal cell growth and protect the cell from DNA damage. Using non-transformed embryonic fibroblasts, we provide evidence of a molecular link between the regulation of survivin transcription and the RB/E2F family of proteins. We demonstrate that both pRB and p130 can interact with the survivin promoter and can repress survivin transcription. We also show that the E2F activators (E2F1, E2F2, and E2F3) can bind to the survivin promoter and induce survivin transcription. Genetically modified cells that harbor deletions in various members of the RB/E2F family confirm our data from the wild-type cells. Our findings implicate several members of the RB/E2F pathway in an intricate mechanism of survivin gene regulation that, when genetically altered during the process of tumorigenesis, may function within cancer cells to aberrantly alter survivin levels and enhance tumor progression. 

Retracted: No

PubPeer comments:
 Figures 3A and 4A. Much more similar than you would expect. https: imgur.com y17hAvU ,
Inducing apoptosis and enhancing chemosensitivity to gemcitabine via RNA interference targeting Mcl-1 gene in pancreatic carcinoma cell
Authors: Ke Dong
Hui-Zhong Zhang
San-Hua Wei
Xi Wang
Qing Zhang
Rui Wang
Jian-Jun Shen
Bin Li
Fang Lin
Journal: Cancer Chemotherapy and Pharmacology (2008)
Discipline: CLINICAL MEDICINE
Keywords: Chemotherapy resistance; Pancreatic carcinoma; Mcl-1; Apoptosis; Chemosensitivity
Affiliations: Research Center, Tangdu Hospital, Fourth Military Medical University, Xinsi Road, 710038, Xi'an, Shaanxi, China.

Abstract:  Purpose: Resistance to chemotherapy is a major cause of treatment failure and poor prognosis in pancreatic carcinoma. Myeloid cell leukemia-1 (Mcl-1) is highly up-regulated in pancreatic carcinoma and is associated with the anti-apoptosis and the resistance to chemotherapy drugs. Suppression of Mcl-1 would be an approach to induce apoptosis and enhance the chemosensitivity. Methods: In this study, three pancreatic cancer cell lines (PANC-1, BxPC-3 and SW1900) stably expressing shRNAs targeting Mcl-1 gene were established and gene expression inhibition was assessed by Real-Time QPCR and Western blotting. The effects of Mcl-1 downregulation mediated by RNAi were explored in vitro and in vivo. Results: We showed that the specific downregulation of Mcl-1 strikingly inhibited cell growth, colony formation, cell cycle arrest and induced apoptosis in pancreatic cancer cells in vitro, and markedly decreased the tumorigenicity in a mouse xenograft model. Moreover, knockdown of Mcl-1 significantly increased the chemosensitivity to Gemcitabine in pancreatic carcinoma cells. Conclusions: Our data suggests that the specific downregulation of Mcl-1 by RNAi is a promising approach to induce apoptosis and enhance the chemosensitivity for pancreatic carcinoma gene therapy. 

Retracted: No

PubPeer comments:
null, 
 I was Peer 1. The concern voiced above was reported to the journal together with 28 other papers in the summer of 2015, with a friendly reminder in April 2017, but no answer. With the exception of one paper, the journal did not correct or retract a single paper from this set. Could the authors please clarify if the journal contacted them back in 2015? , 
 An additional concern about Figure 2B. * Some lanes look more similar to each other than expected. Some are in mirror image. ![file] , 
 An additional finding for Figure 6A. * Purple and pink boxes: The left two panels appear to share some similar groups of data points, while other parts look different. ![file] ,