PReD-Bench/PRed-Bench huggingface dataset:
Role of miR‐106‐mediated mitogen‐activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension
Authors: Zhihui Wang
Ping Sun
Xiufang Bao
Yuying Tian
Limeng Song
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MAP kinase signaling system; inflammation; liver; microRNAs; oxidative stress
Affiliations: Department of Obstetrics and GynecologyAffiliated Hospital of Inner Mongolia University for the Nationalities Tongliao China, Department of Obstetrics and GynecologyInner Mongolia People's Hospital Hohhot China, Department of PathologyAffiliated Hospital of Inner Mongolia University for the Nationalities Tongliao China

Abstract:  We aim to investigate the role of miR-106-mediated mitogen-activated protein kinase (MAPK) signaling pathway in oxidative stress (OS) injury and inflammatory infiltration in the liver of the mouse with gestational hypertension (GH). Ninety specific pathogen-free mice (Kunming species) during middle to late gestation were selected for the study. Fifteen mice were used as control, while the rest were used for establishing the GH model. The mice were assigned to six groups: normal group (normal gestation), model group (GH model), negative control group (GH model, intravenously injected with negative control vector), miR-106a-mimic group (GH model, intravenously injected with vector overexpressing miR-106a, which mimics the overexpression of endogenous mature miR-106a), SB203580 group (GH model, intravenously injected with MAPK pathway inhibitor SB203580), and miR-106a-mimic+SB203580 group (GH model, intravenously injected with SB203580 and vector overexpressing miR-106a). Fourteen days after electrical stimulation, all the groups except for the normal group had elevated blood pressure vs those on day 0 and 7. Compared with the normal group, the other groups had lower levels of miR-106a expression, nitric oxide, nitric oxide synthase, catalase, superoxide dismutase, S cell ratio, and interleukin-4 (IL-4) and IL-10 in the serum and liver as opposed to increased levels of blood pressure, p38MAPK mRNA expression, p-p38MAPK positive expression rate, protein expressions of p-p38MAPK, p-ERK, and p-JNK, H2 O2 and malondialdehyde in liver, G0/G1 cell ratio, apoptosis rate, and IL-6, interferon-γ (IFN-γ), and IFN-α in the serum and liver (all P &lt; .05). The miR-106 overexpression or inhibiting MAPK signaling pathway can attenuate OS injury and inflammatory response in the liver of the mouse with GH, and the effect can be even better if both miR-106a overexpression and inhibiting MAPK pathway are applied. In conclusion, miR-106a overexpression can inhibit OS injury and inflammatory infiltration in the liver of the mouse with GH by mediating MAPK signaling pathway. 

Retracted: No

PubPeer comments:
 The Western blots in this article have repetitive patterns in the background (seen by increasing the contrast). This is seen within a blot (e.g. Figure 3C) or between blots (Figure 7B). This paper does not represent any of the three groups of falsified papers from known paper mills. ![file] ,
Nutlin-3 cooperates with doxorubicin to induce apoptosis of human hepatocellular carcinoma cells through p53 or p73 signaling pathways
Authors: Xuan Song
Xianzhi Meng
Tongsen Zheng
Jiabei Wang
Lianxin Liu
Shangha Pan
Hongchi Jiang
Journal: Journal of Cancer Research and Clinical Oncology (2010)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocellular carcinoma; chemotherapy; Doxorubicin; Nutlin-3; p53
Affiliations: Department of General Surgery, First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin 150001, Heilongjiang Province, China.

Abstract:  Purpose: Despite recent advances in chemotherapeutic agents for Hepatocellular carcinoma (HCC) treatment, the results of chemotherapy remain unsatisfactory. Doxorubicin (DOX) still represents the cornerstone in HCC chemotherapy, but resistance and toxicity to normal cells are major obstacles to successful chemotherapy. Therefore, new active agents in HCC chemotherapy and agents that increase the chemosensitivity of HCC cells to DOX are still urgently required. Nutlin-3 is a small-molecule inhibitor that acts to inhibit murine double minute-2 (MDM2) binding to p53 or p73, and subsequently activates p53- or p73-dependent apoptosis signaling pathway. This study was designed to investigate whether Nutlin-3 alters cell toxicity to HCC cells following DNA damage and to assess the suitability of DOX/Nutlin-3 as a chemotherapeutic combination in HCC chemotherapy. Methods: Four human HCC cells were analyzed using cell proliferation assay, apoptosis assay, western blotting, co-immunoprecipitation and siRNA experiments. Anti-tumoral effects of Nutlin-3/DOX targeting the p53/MDM2 and p73/MDM2 pathways were evaluated in HCC cell lines. Results: Nutlin-3 enhances the growth inhibition by DOX and potentates the apoptotic effect in all HCC cell lines with different p53 types. Nutlin-3 acts through the disruption of p53-MDM2 binding in HepG2, and the disruption of p73-MDM2 in Huh-7 and Hep3B cell lines with subsequent activation of the apoptotic pathway, which leads to the increase in chemosensitivity to DOX in HCC cells. Conclusions: Taken together, our findings suggest that Nutlin-3 will be active in the treatment of HCC and offers new prospects for overcoming DOX resistance. 

Retracted: No

PubPeer comments:
 Two flow cytometry panels presented in Figure 2A look unexpected similar to each other, marked with blue boxes. ![file] , 
 The MDM2 panel in HepG2 cells (after horizontal flip and contrast enhancement) appears to show unexpected similarities to the MDM2 panel in Hep3B cells ![file] , 
 ![file] there are several horizontal flips and contrast-enhanced areas ,
Protective effect of ganoderic acid against the streptozotocin induced diabetes, inflammation, hyperlipidemia and microbiota imbalance in diabetic rats
Authors: Lei Ren
Journal: Saudi Journal of Biological Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 3T3-L1 preadipocytes; Ganoderic acid; Peroxisome proliferator-activated receptor; Type I diabetes mellitus.
Affiliations: Department of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City 450002, China.

Abstract:  Diabetes mellitus (DM) is a metabolic disorder with numerous symptoms categorized via serves hyperglycemia effect along with altered fat, protein and carbohydrate metabolism mainly resultant from defects in insulin action/secretion or both. The aim of the current experimental study was to comfort the neuroprotective effect of ganoderic acid against the streptozotocin (STZ)-induced type I diabetes mellitus in mice and explore the underlying mechanism. Differentiation of 3T3-L1 preadipocytes effect; hepatic and glucose consumption effect of ganoderic acid was estimated on HepG2 cell lines and peroxisome proliferator-activated receptor (PPAR). FFA content was estimated in adipose and hepatic tissues. Ganoderic acid induced the 3T3-L1 preadipocytes differentiation. The mRNA expression of PPAR was increased in the high glucose-treated group in HepG2 and ganoderic acid treatment down-regulated the mRNA expression of PPAR. Ganoderic acid exhibited the inhibitory effect of α-glucosidase and α-amylase. Ganoderic acid demonstrated the reduced blood glucose and increase insulin level and also reduced the free fatty in hepatic and adipose tissue. Histopathological study showed the enhancement of β-cells in ganoderic acid-treated mice. Finally, their prebiotic effects on gut microbiota were illustrated via enhancing the population of diabetes resistant bacteria and also reducing the quantity of diabetes sensitive bacteria. Ganoderic acid attenuated STZ induced T1DM in mice via inflammatory pathways. 

Retracted: No

PubPeer comments:
 Images in Figure 11 and 12 appear to be appear to be repeated repeated. *** ![file] , 
 The author appears to have confused whether Swiss Albino mice or rats were the subject of this study. Could the author please clarify this point? ![file] ![file] ,
Multiple cytotoxic effects of gamabufotalin against human glioblastoma cell line U-87
Authors: Haiyu Zhao
Mari Okazaki
Nan Si
Bo Yuan
Baolin Bian
Ryota Shimada
Kang Xu
Hideki Hayashi
Norio Takagi
Lingyu Han
Journal: Chemico-Biological Interactions (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Autophagy; G(2)/M arrest; Gamabufotalin; Glioblastoma; Metastasis
Affiliations: Department of Applied Biochemistry, Tokyo University of Pharmacy & Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo, 192-0392, Japan; Laboratory of Pharmacology, School of Pharmacy, Faculty of Pharmacy and Pharmaceutical Sciences, Josai University, 1-1 Keyakidai, Sakado, Saitama, 350-0295, Japan. Electronic address: ., Department of Applied Biochemistry, Tokyo University of Pharmacy & Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo, 192-0392, Japan., Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, PR China., Laboratory of Pharmacology, School of Pharmacy, Faculty of Pharmacy and Pharmaceutical Sciences, Josai University, 1-1 Keyakidai, Sakado, Saitama, 350-0295, Japan.

Abstract:  To provide novel insight into approaches designed to combat glioblastoma, the molecular details of the cytotoxicity of gamabufotalin, were investigated in the human glioblastoma cell line U-87. A dose-dependent cytotoxicity was observed in the cells, whereas no detectable toxicity was confirmed in mouse primary astrocytes. LDH leakage was only observed in the cells treated with a relatively high concentration (&gt;80 ng/ml). Downregulation of the expression levels of Aurora B, cdc25A, cdc25C, cdc2, Cyclin B1 and survivin, and upregulation of the expression level of p21 were observed in treated cells and occurred in parallel with G2/M phase arrest. Treatment with gamabufotalin also downregulated the expression level of uPA, CA9, and upregulated the expression level of TIMP3, all of which are closely associated with invasion/metastasis. Autophagy induction was observed in the treated cells and the addition of wortmannin, a potent autophagy inhibitor, significantly rescued U-87 cells. These results indicate that gamabufotalin exhibits cytotoxicity against cancerous glial cells with high potency and selectivity through multiple cytotoxic signaling pathways. The activation of p38 MAPK pathway along with the upregulation of VEGF/VEGFR2 was observed in the treated cells, both of which are likely to be compensatory changes in response to gamabufotalin treatment. Intriguingly, a specific inhibitor of p38 MAPK enhanced the cytotoxicity of the drug, suggesting an important prosurvival role for p38 MAPK. We thus suggest that developing a new combination regimen of gamabufotalin plus a p38 MAPK inhibitor and/or inhibitors for VEGF/VEGFR could improve the efficacy of the drug, and may provide more therapeutic benefits to patients with glioblastoma. 

Retracted: No

PubPeer comments:
 beta-actin bands of Figure 6, 8A, and 9A are identical: ![file] ,
miR‐365 secreted from M2 Macrophage‐derived extracellular vesicles promotes pancreatic ductal adenocarcinoma progression through the BTG2/FAK/AKT axis
Authors: Hao Xu
Jianfeng Yi
Hui Zhang
Zhengfeng Wang
Xin Li
Chunlu Dong
Wence Zhou
Long Miao
Journal: Journal of Cellular and Molecular Medicine (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: BTG2; FAK/AKT pathway; cell invasion; extracellular vesicles; macrophages
Affiliations: The First Clinical Medical College, Lanzhou University, Lanzhou, China., Department of General Surgery, the First Hospital of Lanzhou University, Lanzhou, China.

Abstract:  Clinical and experimental evidence indicates that tumour-associated macrophages support cancer progression. Moreover, macrophage-derived extracellular vesicles (EVs) are involved in pathogenesis of multiple cancers, yet the functions of molecular determinants in which have not been fully understood. Herein, we aim to understand whether macrophage modulates pancreatic ductal adenocarcinoma (PDAC) progression in an EV-dependent manner and the underlying mechanisms. microRNA (miR)-365 was experimentally determined to be enriched in the EVs from M2 macrophages (M2-EVs), which could be transferred into PDAC cells. Using a co-culture system, M2-EVs could enhance the proliferating, migrating and invading potentials of PDAC cells, while inhibition of miR-365 in M2-EVs could repress these malignant functions. B-cell translocation gene 2 (BTG2) was identified to be a direct target of miR-365, while the focal adhesion kinase (F/ATP)-dependent tyrosine kinase (AKT) pathway was activated by miR-365. We further demonstrated that overexpression of BTG2 could delay the progression of PDAC in vitro, whereas by impairing BTG2-mediated anti-tumour effect, M2-EV-miR-365 promoted PDAC progression. For validation, a nude mouse model of tumorigenesis was established, in which we found that targeting M2-EV-miR-365 contributed to suppression of tumour growth. Collectively, M2-EVs carry miR-365 to suppress BTG2 expression, which activated FAK/AKT pathway, thus promoting PDAC development. 

Retracted: No

PubPeer comments:
 Figure 3F and 4D. * Red boxes: Bands in the ADD1 C2C12 panel in Figure 3F looks unexpectedly similar to bands in the rotated cyclin D1 C2C12 panel in Figure 4D. 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] ,
Parkin deficiency prevents chronic ethanol-induced hepatic lipid accumulation through β-catenin accumulation
Authors: Dong Hun Lee
Jin Tae Hong
Chul Ju Hwang
Mi Hee Park
Youngsoo Kim
Sang Bae Han
Dae Yeon Hwang
Journal: Cell Communication and Signaling (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Alcoholic fatty liver; Parkin; Ubiquitination; β-Catenin.
Affiliations: College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungduk-gu, Cheongju, Chungbuk, 28160, Republic of Korea., Department of Biomaterial Science, Pusan National University, 2, Busandaehak-ro 63beon-gil, Geumjeong-gu, Busan, 46241, Republic of Korea., College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungduk-gu, Cheongju, Chungbuk, 28160, Republic of Korea. .

Abstract:  Background: Alcohol abuse and alcoholism lead to alcohol liver disease such as alcoholic fatty liver. Parkin is a component of the multiprotein E3 ubiquitin ligase complex and is associated with hepatic lipid accumulation. However, the role of parkin in ethanol-induced liver disease has not been reported. Here, we tested the effect of parkin on ethanol-induced fatty liver in parkin knockout (KO) mice with chronic ethanol feeding. Methods: Male wild type (WT) and parkin KO mice (10-12 weeks old, n = 10) were fed on a Lieber-DeCarli diet containing 6.6% ethanol for 10 days. Liver histological, biochemical, and gene-expression studies were performed. Results: Parkin KO mice exhibited lower hepatosteatosis after ethanol consumption. Because several studies reported that β-catenin is a critical factor in ethanol metabolism and protects against alcohol-induced hepatosteatosis, we investigated whether parkin changes β-catenin accumulation in the liver of ethanol-fed mice. Our results show that β-catenin was greatly accumulated in the livers of ethanol-fed parkin KO mice compared to ethanol-fed WT mice, and that parkin binds to β-catenin and promotes its degradation it by ubiquitination. Moreover, the β-catenin inhibitor IWR-1 abrogated the attenuation of ethanol-induced hepatic lipid accumulation by parkin deficiency in the livers of parkin KO mice and parkin siRNA-transfected human hepatic cell line. Conclusions: Parkin deficiency prevents ethanol-induced hepatic lipid accumulation through promotion of β-catenin signaling by failure of β-catenin degradation. 

Retracted: No

PubPeer comments:
 Figure 2A appears to contain two images which overlap but are described as representing different mice. *** ![file] *** ![file] , 
 The livers of Pair-fed WT and Pair-fed KO mice showed normal histological feature. Thus, it seems that an error occurred in the process of selecting representative figure. Therefore, we checked that and uploaded 3 liver H E figures per each group (Pair-fed WT and Pair-fed KO mice). As you can see, the liver of those group showed normal histological feature ![file] , 
 #2 Thank you for responding. Will the authors be contacting the journal? ,
Regiospecific phosphorylation control of the SR protein ASF/SF2 by SRPK1
Authors: Jonathan C Hagopian
Chen-Ting Ma
Gourisankar Ghosh
Xiang-Dong Fu
Joseph A Adams
Journal: Journal of Molecular Biology (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SR proteins; splicing factors; precursor mRNA; spliceosome development; ASF/SF2
Affiliations: Department of Pharmacology, University of California, La Jolla, CA 92093-0636, USA.

Abstract:  SR proteins (splicing factors containing arginine-serine repeats) are essential factors that control the splicing of precursor mRNA by regulating multiple steps in spliceosome development. The prototypical SR protein ASF/SF2 (human alternative splicing factor) contains two N-terminal RNA recognition motifs (RRMs) (RRM1 and RRM2) and a 50-residue C-terminal RS (arginine-serine-rich) domain that can be phosphorylated at numerous serines by the protein kinase SR-specific protein kinase (SRPK) 1. The RS domain [C-terminal domain that is rich in arginine-serine repeats (residues 198-248)] is further divided into N-terminal [RS1: N-terminal portion of the RS domain (residues 198-227)] and C-terminal [RS2: C-terminal portion of the RS domain (residues 228-248)] segments whose modification guides the nuclear localization of ASF/SF2. While previous studies revealed that SRPK1 phosphorylates RS1, regiospecific and temporal-specific control within the largely redundant RS domain is not well understood. To address this issue, we performed engineered footprinting and single-turnover experiments to determine where and how SRPK1 initiates phosphorylation within the RS domain. The data show that local sequence elements in the RS domain control the strong kinetic preference for RS1 phosphorylation. SRPK1 initiates phosphorylation in a small region of serines (initiation box) in the middle of the RS domain at the C-terminal end of RS1 and then proceeds in an N-terminal direction. This initiation process requires both a viable docking groove in the large lobe of SRPK1 and one RRM (RRM2) on the N-terminal flank of the RS domain. Thus, while local RS/SR content steers regional preferences in the RS domain, distal contacts with SRPK1 guide initiation and directional phosphorylation within these regions. 

Retracted: No

PubPeer comments:
 Figure 8B showed undeclared slicing of the gel. Please explain. ![file] Also, The histogram in red in S4D and S4E were identical while having different intensity values, please explain. ![file] , 
 #1 Fig. 8c likewise appears to show undeclared splicing. ![file] ,
Brusatol inhibits amyloid‐β‐induced neurotoxicity in U‐251 cells via regulating the Nrf2/HO‐1 pathway
Authors: HuaWen Xu
YueQi Zhang
Xin Liu
Peng Wang
Wei Gao
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Nrf2/HO-1 pathway; U-251 cells; amyloid-β (Aβ); brusatol (BR); neurotoxicity.
Affiliations: Department of NeurologyZouCheng Branch of Affiliated Hospital of Jining Medical UniversityJining Shandong China, Department of NeurosurgeryZouCheng Branch of Affiliated Hospital of Jining Medical UniversityJining Shandong China, Department of NeurologyWeiFang People's HospitalWeiFang Shandong China, Department of NeurologyLiaoCheng Third People's HospitalLiaoCheng Shandong China

Abstract:  Amyloid-β (Aβ) has been reported to cause oxidative damage of neurons leading to neurotoxicity in a variety of diseases and cancers. As an anticancer drug, brusatol (BR) has been shown to have potent cytotoxic effects on various cancer cell lines. In this study, the effect and mechanism of BR on Aβ-induced neurotoxicity was investigated in U-251 glioma cells. Using the MTT assay, the results suggest that BR ameliorated cell injury induced by Aβ in U-251 cells. After running Hoechst and Western blot assays, BR prevented cell apoptosis induced by Aβ in U-251 cells. In addition, BR inhibited the increased reactive oxygen species and mitochondrial membrane potential levels induced by Aβ in U-251 cells using the DCFH-DA and Rh123 method. Furthermore, BR induced the Nrf2/HO-1 pathway by inhibiting the PI3K/AKT/mTOR pathway to inhibit neurotoxicity elicited by Aβ. These results suggest that brustasol is a valuable potential antitumor drug available for chemotherapy. 

Retracted: No

PubPeer comments:
 Great ! One more reason based drug (meplazumab). Pls drop lopinavir ritonavir, [it has no reason to work] They just mention the Mar 14th [Chinese paper] which suggested that CD147 is a new receptor. meplazumab blocks CD147. But there is [more evidence] that CD147 - and not ACE2 - is the receptor. Including data from monkey [cells infected with SARS-Cov2] - where there is little ACE2, and much more CD147 expression , 
 **Please discard our previous comment** ,
Molecular Mechanisms in Amyotrophic Lateral Sclerosis: The Role of Angiogenin, a Secreted RNase
Authors: Jochen H M Prehn
Isabela M Aparicio-Erriu
Journal: Frontiers in neuroscience (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: RNA binding proteins; RNA metabolism; amyotrophic lateral sclerosis; angiogenin; stress signals.
Affiliations: Department of Physiology and Medical Physics, Centre for the Study of Neurological Disorders, Royal College of Surgeons in Ireland Dublin, Ireland.

Abstract:  Amyotrophic lateral sclerosis is a fatal neurodegenerative disease caused by the loss of motoneurons. The precise molecular and cellular basis for neuronal death is not yet well established, but the contemporary view is that it is a culmination of multiple aberrant biological processes. Among the proposed mechanisms of motoneuron degeneration, alterations in the homeostasis of RNA binding proteins (RBP) and the consequent changes in RNA metabolism have received attention recently. The ribonuclease, angiogenin was one of the first RBPs associated with familial and sporadic ALS. It is enriched in motoneurons under physiological conditions, and is required for motoneuron survival under stress conditions. Furthermore, delivery of angiogenin protects cultured motoneurons against stress-induced injury, and significantly increases the survival of motoneurons in SOD(G93A) mice. In this overview on the role of angiogenin in RNA metabolism and in the control of motoneuron survival, we discuss potential pathogenic mechanisms of angiogenin dysfunction relevant to ALS and other neurodegenerative disorders. We also discuss recent evidence demonstrating that angiogenin secreted from stressed motoneurons may alter RNA metabolism in astrocytes. 

Retracted: No

PubPeer comments:
 References. Kieran, D., Sebastia, S., Greenway, M. J., King, M. A., Connaughton, D., Concannon, C. G., et al. (2008). Control of motoneuron survival by angiogenin. J. Neurosci. 28, 14056u201314061. https: pubpeer.com publications 1FA2EBA4A326D65A49C257E31A0D69 Sebastia, J., Kieran, D., Breen, B., King, M. A., Netteland, D. F., Joyce, D., et al. (2009). Angiogenin protects motoneurons against hypoxic injury. Cell Death Differ. 16, 1238u20131247. https: pubpeer.com publications 7840919D4CFF0760DA9F03D100DEBC ,
LINC00311 promotes cancer stem‐like properties by targeting miR‐330‐5p/TLR4 pathway in human papillary thyroid cancer
Authors: Liyang Zhu
Wei Liang
Li Zhang
Wei Zhang
Yu Gao
Fan Wang
Lei Xu
Mei Kang
Journal: Cancer Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: LINC00311; MiR-330-5p; TLR4; papillary thyroid cancer; spheroid formation
Affiliations: Department of Radiotherapy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China., Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.

Abstract:  Growing evidence has suggested that long noncoding RNAs (lncRNAs) play an essential role in the progression of papillary thyroid cancer (PTC). LncRNA LINC00311 was found to be able to regulate many cellular process in several diseases. However, the function and regulatory mechanism of LINC00311 remains unclear in PTC. In the present study, the results showed that the expression of LINC00311 was upregulated in PTC tissues and cells. Furthermore, knockdown of LINC00311 dramatically suppressed spheroid formation, proliferation, migration, and invasion in PTC cells in vitro. Mechanistic investigations revealed that LINC00311 was negatively correlated with the expression of miR-330-5p, meanwhile, TLR4 was a direct target of miR-330-5p. In addition, rescue assays further determined that LINC00311 contributed to the progression of PTC through regulating TLR4 expression. Taken together, these findings indicated that LINC00311 could promote cancer stem-like properties by targeting miR-330-5p/TLR4 pathway in PTC. 

Retracted: No

PubPeer comments:
 An image in Figure 7D overlaps with and image in Figure 7B in another paper: April 2019 Cancer Management and Research DOI:10.2147 CMAR.S193647, discussed here: https: pubpeer.com publications 1A5FFEED4DB9B3FE7AB47DA0A75511 Oddly, there does not appear to be any overlap in authorship or institutional affiliation. However, as the images only partially overlap, it appears that whomever prepared the papers had access to the original data. Could the authors please explain? *** ![file] ,
Effect of Thymoquinone on Acute Kidney Injury Induced by Sepsis in BALB/c Mice
Authors: Lu-Lu Xu
Hong-Yang Liu
Yu-Hua Hao
Si-Xu Liu
Li-Peng Guo
Qin Yang
Xiao-Qing Zhang
Journal: BioMed Research International (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Acute kidney injury; Sepsis; COVID-19; Thymoquinone; Nigella sativa seeds
Affiliations: Department of Cardiology, Dalian Third People’s Hospital Affiliated to Dalian Medical University, No. 40 Qianshan Road, Dalian, China, Department of Internal Medicine, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China, Department of Heart Intensive Care Unit, The First Affiliated Hospital of Dalian Medical University, No. 193 Lianhe Road, Dalian, China, Department of Infection, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China

Abstract:  Acute kidney injury (AKI) is a common complication of sepsis and has also been observed in some patients suffering from the new coronavirus pneumonia COVID-19, which is currently a major global concern. Thymoquinone (TQ) is one of the most active ingredients in Nigella sativa seeds. It has a variety of beneficial properties including anti-inflammatory and antioxidative activities. Here, we investigated the possible protective effects of TQ against kidney damage in septic BALB/c mice. Eight-week-old male BALB/c mice were divided into four groups: control, TQ, cecal ligation and puncture (CLP), and TQ+CLP. CLP was performed after 2 weeks of TQ gavage. After 48 h, we measured the histopathological alterations in the kidney tissue and the serum levels of creatinine (CRE) and blood urea nitrogen (BUN). We also evaluated pyroptosis (NLRP3, caspase-1), apoptosis (caspase-3, caspase-8), proinflammatory (TNF-α, IL-1β, and IL-6)-related protein and gene expression levels. Our results demonstrated that TQ inhibited CLP-induced increased serum CRE and BUN levels. It also significantly inhibited the high levels of NLRP3, caspase-1, caspase-3, caspase-8, TNF-α, IL-1β, and IL-6 induced by CLP. Furthermore, NF-κB protein level was significantly decreased in the TQ+CLP group than in the CLP group. Together, our results indicate that TQ may be a potential therapeutic agent for sepsis-induced AKI. 

Retracted: No

PubPeer comments:
 Figure 1: Control and TQ+CLP panels are the same image; even the arrow points to the same element (please see blue rectangles in the attached image). Could the authors provide the original photographs? ![file] , 
 Thank you for helping us find this problem. The pictures in the blue rectangles are the same. But the reason should be that there were problems with the typesetting or proof in the final printing, because the Figure 1 were not like this when the first submission and the article was received, mainly because the TQ+CLP group is not the same picture. Please see the Figure 1 in the attached images. Do we should be to contact the editor of the magazine to make changes? ![file] ![file] , 
 #2 Yes. Please contact the journal to work out a corrigendum. , 
 #1 Dear Hedyotis Flavescens We contacted the editor of the magazine and to publish an erratum to Figure 1.![file] ,
MicroRNA‑432‑5p inhibits cell migration and invasion by targeting CXCL5 in colorectal cancer
Authors: Zuowei Hu
Yuefeng Kong
Lingyi Li
Man Luo
Journal: Experimental and Therapeutic Medicine (2021)
Discipline: CLINICAL MEDICINE
Keywords: CXCL5; colorectal cancer; invasion; miR-432-5p; migration.
Affiliations: Department of Oncology, Wuhan No. 1 Hospital, Wuhan, Hubei 430022, P.R. China, Department of Radiology, Wuhan Fourth Hospital, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China, Department of Dermatology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China

Abstract:  MicroRNAs (miRNAs) play an important role in the occurrence and development of colorectal cancer (CRC). Evidence shows that miR-432-5p expression is decreased in various tumors and cancer cell lines. miR-432-5p can inhibit tumor invasion and metastasis, but its role in colorectal cancer is unclear. The present study demonstrated that miR-432-5p expression was decreased in colorectal cancer tissue and cell lines, and is negatively associated with invasion classification, lymph node metastasis and Tumor-Node-Metastasis stage. Kaplan-Meier survival analysis showed that low miR-432-5p expression was associated with a poor survival rate in patients with CRC. In addition, SW480 and HT-29 cells transfected with miR-432-5p mimics had decreased migration and invasion abilities, whereas miR-432-5p inhibitors had the opposite effect. The expression of C-X-C motif chemokine ligand 5 (CXCL5), a direct target of miR-432-5p, was negatively associated with miR-432-5p expression. When CXCL5 was introduced into miR-432-5p mimic-transfected SW480 and HT-29 cells, miR-432-5p-mediated inhibition of CRC migration and invasion was reversed. Thus, the present results suggest that miR-432-5p can inhibit the migration and invasion of CRC cells by targeting CXCL5. 

Retracted: No

PubPeer comments:
 Figure 2D and 4D. * Some areas look more similar to each other than expected. Note that In Figure 2D the similarities are only partial, where some cells look similar but not all. ![file] ,
Ultrasound assisted-phytofabricated Fe3O4 NPs with antioxidant properties and antibacterial effects on growth, biofilm formation, and spreading ability of multidrug resistant bacteria
Authors: Mehran Alavi
Naser Karimi
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Antibacterial; Fe3O4 NPs; MDR bacteria; antibiofilm; dendrimer shape
Affiliations: a Department of Nanobiotechnology, Faculty of Science, Razi University , Kermanshah , Iran., b Department of Biology, Faculty of Science, Razi University , Kermanshah , Iran.

Abstract:  Complicated issue in infectious illnesses therapy is increasing of multidrug resistant (MDR) bacteria and biofilms in bacterial infections. In this way, emerging of nanotechnology as a new weapon specifically in the cases of metal nanoparticle (MNPs) synthesis and MNPs surface modification has obtained more attention. In this study, ultrasound-assisted green synthesis method was utilized for the preparation of Fe3O4 NPs with novel shape (dendrimer) through leaf aqueous extract of Artemisia haussknechtii Boiss. Ultraviolet-visible spectroscopy, energy dispersive X-ray spectroscopy (EDX), Fourier transform infrared spectroscopy (FT-IR), scanning electron microscopy (SEM), atomic force microscopic (AFM), X-ray diffraction (XRD) techniques were applied for MNPs physicochemical characterization. Also, disc diffusion assay, minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), planktonic and biofilm morphology of three pathogenic bacteria involving Serratia marcescens ATCC 13880, Escherichia coli ATCC 25922, and methicillin-resistant Staphylococcus aureus (MRSA) were evaluated upon treatment of Fe3O4 NPs as antiplanktonic and antibiofilm analysis. Results showed efficient antiplanktonic and antibiofilm activities of biosynthesized Fe3O4 NPs with average diameter size of 83.4 nm. Reduction in biofilm formation of S. aureus ATCC under Fe3O4 NPs stress was significant (66%) in higher MNPs concentration (100 μg/mL). In addition, as first report, spreading ability of S. aureus as important factor in colony expansion on culture medium was reduced by increasing of Fe3O4 NPs. Present study demonstrates striking antiplanktonic, antibiofilm, antispreading mobility and antioxidant aspects of one-pot biosynthesized Fe3O4 NPs with novel shape. 

Retracted: No

PubPeer comments:
 Images in Figure 14c and 14c appear to overlap. *** ![file] *** Full figure ![file] ,
MiR-124 changes the sensitivity of lung cancer cells to cisplatin through targeting STAT3
Authors: C Tang
F Ge
M-M Qi
X-J Chen
J Ma
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-124; drug resistance; non-small cell lung cancer; STAT3; cisplatin
Affiliations: School of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, China. .

Abstract:  Objective: To investigate the role of micro ribonucleic acid (miR)-124 in drug resistance of non-small cell lung cancer (NSCLC), and to explore its underlying mechanism. Materials and methods: The expression levels of miR-124 and signal transducer and activator of transcription 3 (STAT3) in maternal A549 cells and cisplatin-resistant A549/DDP cells were detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. A549 and A549/DDP cells were transfected with miR-124 mimics and miR-124 negative control (NC), respectively. Changes in the expression of STAT3 were detected via qRT-PCR and Western blotting. Meanwhile, the sensitivity of cells transfected with miR-124 mimics to cisplatin was detected via methyl thiazolyl tetrazolium (MTT) assay. The effects of miR-124 on the apoptosis, invasion and metastasis of cells were detected via flow cytometry, wound healing assay and transwell assay, respectively. Moreover, wild-type and mutant-type STAT3 luciferase reporter plasmids were co-transfected with miR-124 mimics or miR-124 NC. Luciferase activity was analyzed using the dual-luciferase reporter gene assay. Results: QRT-PCR and Western blotting revealed that the expression level of miR-124 in A549/DDP cells was significantly lower than that of A549 cells. However, the expression level of STAT3 in A549/DDP cells was significantly higher than that of A549 cells. Overexpression of miR-124 remarkably reduced the expression level of STAT3 in A549/DDP cells, increased the sensitivity of A549/DDP cells to cisplatin, and inhibited the invasion and metastasis capacities of cells. In addition, luciferase reporter gene assay demonstrated that miR-124 could negatively regulate the protein expression of STAT3 by binding to its 3'-untranslated region (UTR). Conclusions: MiR-124 regulates the sensitivity of NSCLC to cisplatin. Moreover, it inhibits the invasion and metastasis capacities through targeting STAT3, which can serve as a therapeutic target for cisplatin-based chemotherapy resistance of NSCLC. 

Retracted: No

PubPeer comments:
 Figure 3. The two panels appear to share some data points. ![file] ,
Acquired cellular resistance to flavopiridol in a human colon carcinoma cell line involves up-regulation of the telomerase catalytic subunit and telomere elongation. Sensitivity of resistant cells to combination treatment with a telomerase inhibitor
Authors: Lloyd R Kelland
Christopher M Incles
Stephen Neidle
Christoph M Schultes
Journal: Molecular Pharmacology (2003)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Flavopiridol; cyclin-dependent kinases; transcription; P-TEFb; acquired resistance
Affiliations: The School of Pharmacy, 29-39 Brunswick Square, London WC1N 1AX, UK. 

Abstract:  Flavopiridol is a broad-spectrum inhibitor of cyclin-dependent kinases and of global transcription via the inhibition of positive transcription elongation factor b (P-TEFb). Although flavopiridol is currently undergoing phase II clinical trials, acquired cellular resistance to the compound during treatment is a potential problem, as it is with almost all current anticancer agents. A HCT116 human colon carcinoma cell line with an acquired 8-fold resistance to flavopiridol has been established. We report here that there are changes in these resistant cells in terms of telomere length and telomerase activity, whereas no change in the expression of the P-TEFb subunits CDK9, cyclin T1, cyclin T2a, or cyclin T2b was observed. The level of mRNA expression for the telomerase catalytic subunit hTERT was increased over 2-fold in the resistant cells, and mean telomere length was found to be 2 kb longer than the parental length, although telomerase activity was unchanged. The level of mRNA expression for the telomeric binding protein Pot1 was also increased. We also report that treatment of HCT116 cells with a combination of the G-quadruplex interacting telomerase inhibitor BRACO-19 and flavopiridol results in a 3-fold decrease in population doubling and prevents recovery from treatment with either compound alone. Treatment of flavopiridol-resistant cells with BRACO-19 alone also led to rapid inhibition of cell growth, which is not observed in the parental line. The finding that only the resistant line, with up-regulated telomerase, responds to this G-quadruplex inhibitor is consistent with the hypothesis that the mechanism of BRACO-19 down-regulation of cell growth directly involves the targeting of telomeres and telomerase. 

Retracted: No

PubPeer comments:
 Figure 4. Much more similar than expected. ![file] ,
The Source of Glycolytic Intermediates in Mammalian Tissues
Authors: Wenyun Lu
Tara TeSlaa
Xi Xing
Sheng Hui
Zhaoyue Zhang
Xincheng Xu
Lin Wang
Joshua D Rabinowitz
Connor S R Jankowski
Caroline R Bartman
Journal: Cell Metabolism (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: compartmentalized metabolism; glucose homeostasis; glycogen; glycolysis; glycolytic intermediates
Affiliations: Lewis Sigler Institute for Integrative Genomics and Department of Chemistry, Princeton University, Washington Road, Princeton, NJ 08544, USA., Lewis Sigler Institute for Integrative Genomics and Department of Chemistry, Princeton University, Washington Road, Princeton, NJ 08544, USA; Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health, 655 Huntington Avenue, Boston, MA 02115, USA., Lewis Sigler Institute for Integrative Genomics and Department of Chemistry, Princeton University, Washington Road, Princeton, NJ 08544, USA. Electronic address: .

Abstract:  Glycolysis plays a central role in organismal metabolism, but its quantitative inputs across mammalian tissues remain unclear. Here we use 13C-tracing in mice to quantify glycolytic intermediate sources: circulating glucose, intra-tissue glycogen, and circulating gluconeogenic precursors. Circulating glucose is the main source of circulating lactate, the primary end product of tissue glycolysis. Yet circulating glucose highly labels glycolytic intermediates in only a few tissues: blood, spleen, diaphragm, and soleus muscle. Most glycolytic intermediates in the bulk of body tissue, including liver and quadriceps muscle, come instead from glycogen. Gluconeogenesis contributes less but also broadly to glycolytic intermediates, and its flux persists with physiologic feeding (but not hyperinsulinemic clamp). Instead of suppressing gluconeogenesis, feeding activates oxidation of circulating glucose and lactate to maintain glucose homeostasis. Thus, the bulk of the body slowly breaks down internally stored glycogen while select tissues rapidly catabolize circulating glucose to lactate for oxidation throughout the body. 

Retracted: No

PubPeer comments:
 I m confused by Supplemental Figure 4B-C. They say glucose and lactate labeling is basically nothing relative to liver glycogen but in the raw data, at 24H serum glucose is 8%, serum lactate is 7% and liver glycogen is 15%. Does that not mean that serum glucose is roughly 50% labeled relative to liver glycogen?? ![file] ,
Reversible formation of on-pathway macroscopic aggregates during the folding of maltose binding protein
Authors: C Ganesh
R Varadarajan
J B Udgaonkar
F N Zaidi
Journal: Protein Science (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Maltose binding protein; protein folding; export studies; macroscopic aggregates; refolding
Affiliations: Molecular Biophysics Unit, Indian Institute of Science, Bangalore 560 012, India.

Abstract:  Maltose binding protein (MBP) is widely used as a model for protein folding and export studies. We show here that macroscopic aggregates form transiently during the refolding of MBP at micromolar protein concentrations. Disaggregation occurs spontaneously without any aid, and the refolded material has structure and activity identical to those of the native, nondenatured protein. A considerable fraction of protein undergoing folding partitions into the aggregate phase and can be manually separated from the soluble phase by centrifugation. The separated MBP precipitate can be resolubilized and yields active, refolded protein. This demonstrates that both the soluble and aggregate phases contribute to the final yield of refolded protein. SecB, the cognate Escherichia coli cytosolic chaperone in vivo for MBP, reduces but does not entirely prevent aggregation, whereas GroEL and a variety of other control proteins have no effect. Kinetic studies using a variety of spectroscopic probes show that aggregation occurs through a collapsed intermediate with some secondary structure. The aggregate formed during refolding can convert directly to a near native state without going through the unfolded state. Further, optical and electron microscopic studies indicate that the MBP precipitate is not an amyloid. 

Retracted: No

PubPeer comments:
 Compare Euphytica Fig. 5 and Table 1 with Acta Hortic Fig. 2 and Table 1 The 2009 paper does not cite the 2007 paper. DOI: 10.1007 s10681-007-9382-x (copyright = Springer Science + Business Media) DOI: 10.17660 ActaHortic.2009.814.16 (copyright = International Society for Horticultural Science) https: imgur.com a Hw5IFfL https: imgur.com a XI1rrDY , 
 https: retractionwatch.com 2020 10 05 almond-no-joy-plant-geneticist-in-iran-up-to-at-least-six-retractions ,
lncRNA LSINCT5 Regulates miR-20a-5p/XIAP to Inhibit the Growth and Metastasis of Osteosarcoma Cells
Authors: Hao Mo
Shi-An Liao
Ju-Liang He
Jian Guan
Xin-Li Zhan
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: LSI<a href="http://clinicaltrials.gov/show/NCT5" title="See in ClinicalTrials.gov">NCT5</a>; growth; invasion; lncRNA; miR-20a-5p
Affiliations: Department of Spine and Osteopathy Ward, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Province, People's Republic of China., Department of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi Province, People's Republic of China.

Abstract:  Background: More and more evidence has shown that non-coding RNA (ncRNA), including long ncRNA (lncRNA) and micro RNA (miRNA), plays a crucial regulatory role in osteosarcoma (OS). Previously, we revealed a Rho-related coiled coil incorporating protein kinase 1(XIAP). A transfer-related gene is negatively regulated by microRNA-20a-5p (miR-20a-5p) and plays the role of oncogene in OS. It is not clear if any lncRNA is involved in the axial upstream of miR-20a-5p/XIAP. Methods: Expression of LSINCT5 and miR-20a-5p/XIAP in OS tissues was determined through qRT-PCR (qP). The proliferation and migration/invasion activity of OS cells were tested through CCK-8/and transwell assay, respectively. The changes on expression of XIAP were examined through qRT-PCR and Western blot (WB). Targeted binding between LSINCT5, miR-20a-5p, and XIAP has been verified using dual luciferase reporter gene analysis, RNA Immunoprecipitation (RIP), and RNA pull-down experiments. The effect of LSINCT5 on tumor growth was determined by tumor allograft test. Results: In this study, elevated LSINCT5 was found in OS tissue samples and OS cell strains, and the increased LSINCT5 was strongly related to the adverse prognosis of clinical patients. Functional assays showed that inhibition of LSINCT5 could up-regulate miR-20a-5p-mediated OS cells proliferation and metastasis. WB analysis and qP analysis showed that LSINCT5 regulated XIAP by mediating miR-20a-5p. Further cell behavior experiments showed that LSINCT5 acted as a miR-20a-5p sponge to inhibit proliferation and metastasis caused by XIAP. Finally, the results of animal models in vivo showed that LSINCT5 could regulate the tumor growth of OS. Conclusion: LncRNA LSINCT5 acts as an oncogene and promotes XIAP mediated growth and metastasis as competitive endogenous RNA (ceRNA) in OS. 

Retracted: Yes

PubPeer comments:
 In some of the micrographs in this article, patterns are repeated and lined up in the same direction. Please see the example from Figure 6 I am wondering if the authors are sure they put the correlation curve correct? Based on the distribution of data points, it looks odd. There are also a lot of errors and misunderstandings in the text. Examples are shown from Materials and Methods. ![file] ![file] ,