PReD-Bench/PRed-Bench huggingface dataset:
Exosomal lncRNA UCA1 modulates cervical cancer stem cell self-renewal and differentiation through microRNA-122-5p/SOX2 axis
Authors: Mei Ji
Zhihui Gao
Qianqing Wang
Xiaoke Su
Xiangcui Guo
Li Li
Journal: Journal of Translational Medicine (2021)
Discipline: CLINICAL MEDICINE
Keywords: Cervical cancer stem cells; Exosomes; LncRNA UCA1; MicroRNA-122-5p; Proliferation
Affiliations: Department of Gynecology, Xinxiang Central Hospital, NO. 56 Jinsui Road, Xinxiang, 453000, Henan, China., Department of Gynecology, Xinxiang Central Hospital, NO. 56 Jinsui Road, Xinxiang, 453000, Henan, China. ., Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China.

Abstract:  Background: There is growing evidence discussing the role of long non-coding RNAs (lncRNAs) in cervical cancer (CC). We performed this study to explore the impact of exosomal lncRNA urothelial cancer-associated 1 (UCA1) in CC stem cells by sponging microRNA-122-5p (miR-122-5p) and regulating SOX2 expression. Methods: CC stem cells (CD133+CaSki) and exosomes were extracted and identified. The synthesized UCA1- and miR-122-5p-related sequences were transfected into CaSki cells, CaSki cells-derived exosomes were extracted and then co-cultured with CD133+CaSki cells. The functional roles of UCA1 and miR-122-5p in self-renewal and differentiation ability of CC stem cells were determined using ectopic expression, knockdown/depletion and reporter assay experiments. An in vivo experiment was performed to verify the in vitro results. Results: Up-regulated UCA1 and SOX2 and down-regulated miR-122-5p were found in CaSki-Exo. Exosomes promoted invasion, migration, proliferation and restrained apoptosis of CD133+CaSki cells. Silencing UCA1 or up-regulating miR-122-5p degraded SOX2 expression, and reduced invasion, migration and proliferation of CD133+CaSki cells while advanced apoptosis and suppressed the tumor volume and weight in nude mice. Conclusion: Our study provides evidence that CaSki-Exo can promote the self-renewal and differentiation ability of CC stem cells while silencing UCA1 or up-regulating miR-122-5p restrains self-renewal and differentiation of CC stem cells. 

Retracted: No

PubPeer comments:
 Figure 4A: Line #2 and Line #5 appears to be the same image. Could the authors check it please? ![file] , 
 Thank you for your comments. We are checking and will get back to you as soon as possible. , 
 We appreciate your comments about our work. We have checked and found that indeed the images are the same. We apologize for this mistake. We performed extensive experiments with a high number of plants (more than 50 plants), however when preparing the figure, unfortunately this confusion occurred. We have informed the Journal and sent an erratum for publication (Front. Plant Sci. doi: 10.3389 fpls.2020.00201). ,
Purinergic Antagonism Prevents Mitochondrial Dysfunction and Behavioral Deficits Associated with Dopaminergic Toxicity Induced by 6-OHDA in Rats
Authors: Saket Kumar
Sairam Krishnamurthy
Akanksha Mishra
Journal: Neurochemical Research (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Adenosine triphosphate; Brilliant Blue G; Mitochondrial dysfunction; Parkinson’s disease; Purinergic receptors
Affiliations: Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P., 221 005, India., Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P., 221 005, India. .

Abstract:  Purinoceptors are present in neurons, microglia and oligodendrocytes and regulate dopamine (DA) release, striatal-related function and striatal neuronal and DA cells damage. Therefore, purinoceptors may be involved in the pathology of Parkinson's disease (PD) and purinergic antagonism may show neuroprotective effect. The study investigated the role of the non-selective purinergic receptor antagonist pyridoxalphosphate-6-azophenyl-2', 4'-disulfonic acid (PPADS) and a selective purinergic receptor P2X7 receptor antagonist Brilliant Blue G (BBG) against 6-OHDA induced dopaminergic neurotoxicity in rats; while adenosine triphosphate (ATP) was used as a P2X receptor agonist. Behavioral parameters like spontaneous motor activity, narrow beam walk, footprint, bar catalepsy, grip strength and rotarod tests were performed to evaluate motor deficits in PD. Striatal DA contents were estimated as neurochemical measures of PD. Mitochondrial studies and oxidative status were assessed to investigate the mechanism of purinergic system antagonists. Involvement of purinergic receptors in apoptosis was assessed by expressing cytochrome-C, caspase-9 and caspase-3. Both the antagonists not only attenuated 6-OHDA induced motor deficits but also protected against 6-OHDA induced DA depletion in the striatum. Oxidative stress, mitochondrial integrity and dysfunction were attenuated by purinergic antagonists. Further, they attenuated mitochondrial-linked apoptosis as observed by a decrease in expression of cytochrome-C, caspase-9 and caspase-3. Therefore, purinoceptor antagonism shows neuroprotective effect in 6-OHDA induced dopamine toxicity through preservation of mitochondrial bioenergetics and anti-apoptotic activities. 

Retracted: No

PubPeer comments:
 Figure 5a. Some bands appear to look more similar to each other than expected, as shown here with arrows of the same color. ![file] ,
Observation of Resonant Quantum Magnetoelectric Effect in a Multiferroic Metal–Organic Framework
Authors: Shouguo Wang
Liqin Yan
Junzhuang Cong
Ying Tian
Shipeng Shen
Young Sun
Journal: Journal of the American Chemical Society (2016)
Discipline: CHEMISTRY
Keywords: resonant quantum magnetoelectric coupling effect; multiferroic metal-organic framework; spin-canted antiferromagnetic order; ferroelectricity; magnetoelectric coupling
Affiliations: State Key Laboratory of Magnetism, Institute of Physics, Chinese Academy of Sciences , Beijing 100190, PR China.

Abstract:  A resonant quantum magnetoelectric coupling effect has been demonstrated in the multiferroic metal-organic framework of [(CH3)2NH2]Fe(HCOO)3. This material shows a coexistence of a spin-canted antiferromagnetic order and ferroelectricity as well as clear magnetoelectric coupling below TN ≈ 19 K. In addition, a component of single-ion quantum magnets develops below ∼ 8 K because of an intrinsic magnetic phase separation. The stair-shaped magnetic hysteresis loop at 2 K signals resonant quantum tunneling of magnetization. Meanwhile, the magnetic field dependence of dielectric permittivity exhibits sharp peaks just at the critical tunneling fields, evidencing the occurrence of resonant quantum magnetoelectric coupling effect. This resonant effect enables a simple electrical detection of quantum tunneling of magnetization. 

Retracted: No

PubPeer comments:
 ![file] , 
 One more problem: Figure 7C and Figure 9B: The actin blot has been duplicated and presented as something different. ![file] , 
 #2 The 9C version (where the two central lanes are + - si-p53) is presumably the original, what with the overlap between the GAPDH and Actin slices , 
 The original western blot is at least one year older: ![file] I think the University of Kentucky should clean up the mess. Why leave the old invalide papers out there for scientists to waste their time on and citing? , 
 2020 expression of concern. Toxicol Sci.u00a02020u00a0Feb 17. pii: kfaa012. doi: 10.1093 toxsci kfaa012. [Epub ahead of print]Expressionu00a0ofu00a0Concern:  The Dual Roles of c-Jun NH2-Terminal Kinase Signaling in Cr(VI)-Induced Apoptosis in JB6 Cells .Son YO,u00a0Hitron JA,u00a0Cheng S,u00a0Budhraja A,u00a0Zhang Z,u00a0Guo NL,u00a0Lee JC,u00a0Shi X.PMID:u00a032065643u00a0DOI:u00a010.1093 toxsci kfaa012 The Editorial Board ofu00a0Toxicological Sciencesu00a0has been alerted by a reader to concerns regarding the data underlying this paper. Until further notice, this Expression of Concern should be taken to indicate that the data presented in the article named above may not be reliable.u00a0 ,
Long non-coding RNA RPPH1 promotes the proliferation, invasion and migration of human acute myeloid leukemia cells through down-regulating miR-330-5p expression
Authors: Pengyu Zhang
Xingmei Cao
Lu Qian
Xiaorong Ma
Jie Liu
Yinxia Chen
Aili He
Bo Lei
Wanggang Zhang
Journal: EXCLI journal (2019)
Discipline: CHEMISTRY
Keywords: RPPH1; acute myeloid leukemia; long non-coding RNA; miR-330-5p.
Affiliations: Department of Hematology, second Affiliated Hospital of Xi'an Jiaotong University,157 Xiwu Road, Xi'an, Shaanxi, China.

Abstract:  Multiple studies have revealed that the long non-coding RNA RPPH1 (Ribonuclease P RNA Component H1) is involved in disease progression of solid tumors and neurodegenerative diseases. We aimed to explore the functions of RPPH1 in the pathogenesis of acute myeloid leukemia (AML) and the underlying molecular mechanisms. The expression of RPPH1 was examined in blood samples of AML patients and human AML cell lines including THP-1 and HL-60. The microRNAs (miRNAs) targets of RPPH1 were predicted with online tools and validated with the dual luciferase reporter assay. The malignant behaviors of AML cells with lentivirus medicated knockdown of RPPH1 and/or administration of miR-330-5p inhibitor were assessed. Cell proliferation was determined by the CCK-8 and EdU incorporation methods, and cell invasion and migration were assayed with transwell experiments. The effects of RPPH1 knockdown on in vivo tumor growth were evaluated in nude mice with xenografted THP-1 cells. RPPH1 was expressed in the AML tissues and cell lines and its high expression predicted worse overall survival in AML patients. miR-330-5p was validated to be a direct target of RPPH1. Knockdown of RPPH1 suppressed the proliferation, invasion and migration ability of human AML cells, which was partially reversed by additional administration with miR-330-5p inhibitor. RPPH1 knockdown significantly inhibited the growth of xenografted THP-1 tumor in nude mice. Our work highlights the contributions of RPPH1 in promoting AML progression through targeting miR-330-5p, and suggests that the RPPH1/miR-330-5p axis is a potential target for AML treatments. 

Retracted: No

PubPeer comments:
 **Suneet Singh** is the common co-author! ![file] , 
 ![file] , 
 **One common co-author!** ![file] ,
Golgi Phosphoprotein 3 Inhibits the Apoptosis of Human Glioma Cells in Part by Downregulating N-myc Downstream Regulated Gene 1
Authors: Jinqiang Yan
Xiuli Tian
Mengyou Li
Lianqun Zhang
Xueyuan Li
Qingbin Jia
Qingzhe Li
Qingyang Lu
Xin Li
Xingang Li
Journal: Medical Science Monitor (2016)
Discipline: CLINICAL MEDICINE
Keywords: GOLPH3; cell apoptosis; glioma; NDRG1; tumor tissues
Affiliations: Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland)., Department of Respiratory, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland)., , Liaocheng People's Hospital and Clinical School of Taishan Medical University, Liaocheng, Shandong, China (mainland)., Department of Pathology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland)., Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland)., Department of Neurosurgery, Liaocheng People's Hospital, , China (mainland).

Abstract:  BACKGROUND Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development of several human cancers. Our previous study showed that GOLPH3 expression in glioma tissues was related to the severity of the malignancy of the cancer. However, the mechanism by which GOLPH3 affects cell apoptosis is largely unknown. The present study was designed to explore the possible mechanism of GOLPH3 in cell apoptosis. MATERIAL AND METHODS To analyze the biological role of GOLPH3 in glioma cells, we used GOLPH3 small interference RNA in apoptosis of glioma cells. The apoptosis of glioma cells was detected by flow cytometry. The expression level of GOLPH3 and NDRG1 protein was determined by Western blot analyses and immunohistochemical staining, respectively, to evaluate their association with glioma. Tumor tissues were collected from patients with glioma. Normal cerebral tissues were acquired from cerebral trauma patients undergoing internal decompression surgery. RESULTS We confirm that the decrease of GOLPH3 that promotes the apoptosis of glioma cells may be regulated by the activation of NDRG1 and cleaved capcase 3. There was a inverse association between GOLPH3 and NDRG1 in glioma samples. CONCLUSIONS Our findings indicate that GOLPH3 and NDRG1 both play an important role in glioma etiology. Either GOLPH3 or NDRG1 might be a potential candidate for malignant glioma therapy. 

Retracted: No

PubPeer comments:
 Data from Figure 1a,c have been duplicated and presented as something else in Figure 2a,c. ![file] ,
Forsythoside A exerts antipyretic effect on yeast-induced pyrexia mice via inhibiting transient receptor potential vanilloid 1 function
Authors: Hongchang Su
Xiangying Kong
Qingxia Qin
Na Lin
Hongye Wan
Cuiling Liu
Xuan Wu
Journal: International journal of biological sciences (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Fever; Forsythoside A, Mitogen-activated protein kinases.; Transient receptor potential.
Affiliations: Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.

Abstract:  Transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel gated by noxious heat, playing major roles in thermoregulation. Forsythoside A (FT-A) is the most abundant phenylethanoid glycosides in Fructus Forsythiae, which has been prescribed as a medicinal herb for treating fever in China for a long history. However, how FT-A affects pyrexia and what is the underlying molecular mechanism remain largely unknown. Here we found that FT-A exerted apparent antipyretic effect through decreasing the levels of prostaglandin E2 (PGE2) and interleukin 8 (IL-8) in a dose-dependent fashion on the yeast induced pyrexia mice. Interestingly, FT-A significantly downregulated TRPV1 expression in the hypothalamus and dorsal root ganglion (DRG) of the yeast induced pyrexia mice. Moreover, FT-A inhibited IL-8 and PGE2 secretions, and calcium influx in the HEK 293T-TRPV1 cells after stimulated with capsaicin, the specific TRPV1 agonist. Further investigation of the molecular mechanisms revealed that FT-A treatment rapidly inhibited phosphorylation of extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK) and p38 in both yeast induced pyrexia mice and HEK 293T-TRPV1 cells. These results suggest that FT-A may serve as a potential antipyretic agent and the therapeutic action of Fructus Forsythiae on pyretic related disease is, in part, due to the FT-A activities. 

Retracted: No

PubPeer comments:
 Figure 7. Some panels appear to show repetitive elements as marked with boxes of the same color. In addition, in the p-ERK and p-P38 rows, the FT-A 2 and 4 mg kg panels look somewhat similar, as if they were adjacent sections. Is Forsythia the remedy it promises to be? ![file] ,
Long non-coding RNA SNHG4 promotes cervical cancer progression through regulating c-Met via targeting miR-148a-3p
Authors: Walimuni Sandaroo Mendis Abeysekara Wijayakulathilaka
Hanchen Li
Jiang Hong
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cervical cancer; c-Met; lncRNA SNHG4; miR-148a-3p.
Affiliations: Foreign Department-Department of Clinical Medicine, Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russian Federation.

Abstract:  Long non-coding RNA (lncRNA) SNHG4 has been shown to be associated with the development of a variety of cancers. The purpose of this study was to investigate the effect of SNHG4 on cervical cancer (CC) and the corresponding mechanism. The qRT-PCR was used to determine the expressions of SNHG4 and miR-148a-3p in CC cell lines and tissues. Cell apoptosis and proliferation were measured by flow cytometry and MTT assay, respectively. The interaction between SNHG4, miR-148a-3p and c-Met was verified by bioinformatics, dual-luciferase reporter gene and RNA immunoprecipitation (RIP), and the effect of SNHG4 on the growth of CC tumor in vivo was explored. The expression of SNHG4 was increased in both CC cell lines and tissues, while the expression of miR-148a-3p was down-regulated. Meanwhile, silencing SNHG4 remarkably inhibited CC cell proliferation and promoted apoptosis. In addition, miR-148a-3p was a direct target gene of SNHG4, and down-regulation of miR-148a-3p could observably reverse the effect of silencing SNHG4 on the proliferation and apoptosis of CC cells. More importantly, SNHG4 could up-regulate the expression of c-Met by targeting and interacting with miR-148a-3p. Finally, in vivo experiments confirmed that silence SNHG4 down-regulated the expression of c-Met by promoting miR-148a-3p, and ultimately suppressed the growth of CC tumor in vivo. In conclusion, SNHG4 could be used as a competitive endogenous RNA to bind to miR-148a-3p, thereby up-regulating the expression of c-Met and ultimately promoting the progression of CC, which provided a potential therapeutic target for the targeted treatment of CC. 

Retracted: No

PubPeer comments:
 Three panels share most of their points in common and are presumably derived from the same data file, though with differences in gating or filtering. ![file] Panels are from Figs 2e and 4f; from Figs 2E, 3F, 5F, 6E of [Ye et al (2020)] ; and from Figs 2C,4C, 6B of [Li, Li Sun (2019)] . Here in context: ![file] ------------------------------------------ ![] ----------------------------------------- ![] There may be other matching panels, or matches with other papers in this oeuvre. https: docs.google.com spreadsheets d 1X401JM6CcpTSkbKsPsOl20pRKQ-ns1S_J5pTwtBjqPw edit#gid=0 ,
Src-dependent STAT-3-mediated expression of monocyte chemoattractant protein-1 is required for 15(S)-hydroxyeicosatetraenoic acid-induced vascular smooth muscle cell migration
Authors: Nikhlesh K Singh
Gadiparthi N Rao
Manjula Karpurapu
Wayne C Glasgow
Harihara S K Potula
Dong Wang
Dong Van Quyen
Edwards A Park
Venkatesh Kundumani-Sridharan
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 15-LOX1; Vascular smooth muscle cell; Migration; 15(S)-HETE; Src
Affiliations: Department of Physiology, The University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.

Abstract:  To understand the role of human 15-lipoxygenase 1 (15-LOX1) in vascular wall remodeling, we have studied the effect of the major 15-LOX1 metabolite of arachidonic acid, 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), on vascular smooth muscle cell (VSMC) migration both in vitro and in vivo. Among 5(S)-HETE, 12(S)-HETE, and 15(S)-HETE, 15(S)-HETE potentially stimulated more vascular smooth muscle cell (VSMC) migration. In addition, 15(S)-HETE-induced VSMC migration was dependent on Src-mediated activation of signal transducer and activator of transcription-3 (STAT-3). 15(S)-HETE also induced monocyte chemoattractant protein-1 (MCP-1) expression via Src-STAT-3 signaling, and neutralizing anti-MCP-1 antibodies completely negated 15(S)-HETE-induced VSMC migration. Cloning and characterization of a 2.6-kb MCP-1 promoter revealed the presence of four putative STAT-binding sites, and the site that is proximal to the transcription start site was found to be essential for 15(S)-HETE-induced Src-STAT-3-mediated MCP-1 expression. Rat carotid arteries that were subjected to balloon injury and transduced with Ad-15-LOX1 upon exposure to [(3)H]arachidonic acid ex vivo produced 15-HETE as a major eicosanoid and enhanced balloon injury-induced expression of MCP-1 in smooth muscle cells in Src and STAT-3-dependent manner in vivo. Adenovirus-mediated delivery of 15-LOX1 into rat carotid artery also led to recruitment and homing of macrophages to medial region in response to injury. In addition, transduction of Ad-15-LOX1 into arteries enhanced balloon injury-induced smooth muscle cell migration from media to intima and neointima formation. These results show for the first time that 15-LOX1-15(S)-HETE axis plays a major role in vascular wall remodeling after balloon angioplasty. 

Retracted: No

PubPeer comments:
 Figures 1, 2C, 3D: * Green boxes: Three panels appear to be showing the same group of cells, while representing two different experiments * Red boxes: Two panels appear to be showing the same group of cells, while representing two different experiments * Blue boxes: Two panels appear to be showing the same group of cells, but they appear to be representing the different experiments, so this might not be a problem ![file] ,
Speciation and quantitation of precious metals in model acidic leach liquors, theoretical and practical aspects of recycling
Authors: Jérémie Gouyon
Anne Varenne
Fethi Bedioui
Julia Zimmerman
Fanny d&#x27;Orlyé
Sophie Griveau
Journal: Analytical and Bioanalytical Chemistry (2020)
Discipline: CHEMISTRY
Keywords: Electrophoresis; Strategic metals; Thiourea; UV spectrophotometry; Voltammetry.
Affiliations: Chimie ParisTech, CNRS 2027, Institute of Chemistry for Life and Health Sciences, SEISAD, PSL University, 75005, Paris, France., French Environment and Energy Management Agency, 20, Avenue du Grésillé, BP 90406, 49004, Angers Cedex 01, France., Instituto Militar de Engenharia, Rio de Janeiro, RJ, 22290-270, Brazil., Chimie ParisTech, CNRS 2027, Institute of Chemistry for Life and Health Sciences, SEISAD, PSL University, 75005, Paris, France. .

Abstract:  Waste printed circuit boards are a major source of strategic materials such as platinum group metals since they are used for the fabrication of technological devices, such as hard drive discs, capacitors, and diodes. Because of the high cost of platinum, palladium, and gold (&gt; 25 k€/kg), an economic and environmental challenge is their recycling from printed circuit boards that represent around 2% weight of electronic equipment. Hydrometallurgical treatments allow the recovery of these metals in solution, with a high recovery rate for a leaching liquor made of thiourea in hydrochloric acid. So as to develop an efficient recycling process from this leach liquor, one requires the speciation of these strategic metals, as well as their extraction and quantitation in the mixture. For this purpose, platinum, palladium, and gold were dissolved in model leach liquors made of hydrochloric acid and thiourea at low concentration. The identification of metal complexes was determined as a function of thiourea concentration (between 10 μmol/L and 10 mmol/L) by the combination of UV-visible spectrometry, cyclic voltammetry, and for the first time capillary electrophoresis. The electrokinetic method was then applied for the quantitation of trace metal analyses in leach samples from waste printed circuit boards reprocessing, demonstrating its applicability for industrializable recycling applications. Graphical abstract. 

Retracted: No

PubPeer comments:
 Unexpected similarity between some lanes in Fig. 6A (horizontally flipped, stretched, enhanced contrast was applied where necessary to highlight the similarities). Green arrow indicates an unexpected boundary between lanes. ![file] ,
Redistribution of Silencing Proteins from Telomeres to the Nucleolus Is Associated with Extension of Life Span in S. cerevisiae
Authors: D A Sinclair
M Gotta
L Guarente
B K Kennedy
S M Pak
M Murthy
S M Gasser
T Laroche
D S McNabb
K Mills
Journal: Cell (1997)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Sir silencing proteins; AGE locus; long life span; SIR4-42 mutation; Sir protein complex

Abstract:  A prior genetic study indicated that activity of Sir silencing proteins at a hypothetical AGE locus is essential for long life span. In this model, the SIR4-42 mutation would direct the Sir protein complex to the AGE locus, giving rise to a long life span. We show by indirect immunofluorescence that Sir3p and Sir4p are redirected to the nucleolus in the SIR4-42 mutant. Furthermore, this relocalization is dependent on both UTH4 a novel yeast gene that extends life span, and its homologue YGL023. Strikingly, the Sir complex is relocalized from telomeres to the nucleolus in old wild-type cells. We propose that the rDNA is the AGE locus and that nucleolar function is compromised in old yeast cells in a way that may be mitigated by targeting of Sir proteins to the nucleolus. 

Retracted: No

PubPeer comments:
 A room temperature DMA sensor was reported, but there were some results make me confusing and doubt. The respone to 30 ppm DMA was pointed as 6.36 in Fig. 5:![file] But the results in Fig. 6b and 7b were different: ![file] ![file] So which results are the real? ,
Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling
Authors: Thomas J Giordano
Shenglin Li
Peter J Polverini
Jan Kitajewski
Douglas B Chepeha
Jacques Nor
Qinghua Zeng
Cun-Yu Wang
Honglai Zhang
Jong Li
Journal: Cancer Cell (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: tumor angiogenesis; Notch ligand; Jagged1; growth factors; MAPK
Affiliations: Laboratory of Molecular Signaling and Apoptosis, Department of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109, USA.

Abstract:  While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways. 

Retracted: No

PubPeer comments:
 Figure 1A and 4C. Could the authors please clarify the following observation: * Red boxes: The EC+SSC9 H (HGF treated) panel in Figure 1A appears to show an overlap with the EC+SSC9 Jag (Jag expressing) panel in Figure 4C. ![file] ,
ERK kinase phosphorylates and destabilizes the tumor suppressor FBW7 in pancreatic cancer
Authors: Xiangyuan Liu
Liang Liu
Quanxing Ni
Jin Xu
Jing Gao
Dingkong Liang
Haijun Zhou
Shunrong Ji
Yi Qin
Daming Gao
Hu Zhou
Si Shi
Hongli Hu
Bo Zhang
Chen Liu
Paul J Chiao
Wenyan Xu
Jiang Long
Jiang Liu
Xianjun Yu
Journal: Cell Research (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: FBW7; tumor suppressor; pancreatic cancer; ERK activation; KRAS mutations
Affiliations: 1] Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China [2] Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China [3] Pancreatic Cancer Institute, Fudan University, Shanghai 200032, China., Key Laboratory of System Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China., Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China., Department of Molecular and Cellular Oncology, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Abstract:  F-box and WD repeat domain-containing 7 (FBW7) is the substrate recognition component of the Skp1-Cul1-F-box (SCF) ubiquitin ligase complex and functions as a major tumor suppressor by targeting various oncoproteins for degradation. Genomic deletion or mutation of FBW7 has frequently been identified in many human cancers but not in pancreatic ductal adenocarcinoma. Thus it is important to know how the tumor suppressive function of FBW7 is impaired in pancreatic cancer. In this study, we first observed that low FBW7 expression correlated significantly with ERK activation in pancreatic cancer clinical samples, primarily due to KRAS mutations in pancreatic cancer. We further showed that ERK directly interacted with FBW7 and phosphorylated FBW7 at Thr205, which sequentially promoted FBW7 ubiquitination and proteasomal degradation. Furthermore, the phospho-deficient T205A FBW7 mutant is resistant to ERK activation and could significantly suppress pancreatic cancer cell proliferation and tumorigenesis. These results collectively demonstrate how the oncogenic KRAS mutation inhibits the tumor suppressor FBW7, thus revealing an important function of KRAS mutations in promoting pancreatic cancer progression. 

Retracted: No

PubPeer comments:
 In figure1C and table 3, the author indicated that low FBW7 expression was correlated with overall survival (OS) in pancreatic cancer patients (n=86), with P=0.029. ![file] Figure 1C presented the results of KM analysis for FBW7 However, based on TCGA-PAAD datasets, GEPIA predicted NO SIGNIFICANT association between FBW7 and prognosis of PAAD, as follows: GEPIA: http: gepia.cancer-pku.cn detail.php?clicktag=correlation ![file] ![file] NO SIGNIFICANT association between FBW7 and prognosis of PAAD Hence, I question the validity of the SIGNIFICANT result about FBW7. ,
Long non-coding RNA DLEU1 predicts poor prognosis of gastric cancer and contributes to cell proliferation by epigenetically suppressing KLF2
Authors: Xiaobin Li
Ziwen Liu
Yimin Song
Shuting Yu
Zongze Li
Jianchun Xiao
Journal: Cancer Gene Therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: long non-coding RNAs; DLEU1; gastric cancer; tumor size; advanced stage
Affiliations: Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences&Peking Union Medical College, Beijing, 100730, P. R. China., Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences&Peking Union Medical College, Beijing, 100730, P. R. China. .

Abstract:  Currently, accumulating documents have paid great attention to the critical role of long non-coding RNAs. The long non-coding RNAs DLEU1 has been demonstrated to be dysregulated in many solid tumors and hematological malignancies. However, the detailed descriptions about its potential roles and molecular mechanism in gastric cancer (GC) are still blurry. As for our research, it was found out that DLEU1 was observably intensified in GC tissues and cell lines. And highly expressed DLEU1 was relevant to tumor size, advanced stage of pathology and lymph node metastasis in GC patients. Silenced DLEU1 obviously suppressed proliferation via leading to the cell cycle arrest and inducing cell apoptosis of GC. Furthermore, mechanistic experiments uncovered that DLEU1 could recruit LSD1 (lysine specific demethylase 1) to the promoter regions of KLF2 and then suppressed its transcription. In addition, rescue assays revealed that the oncogenic function mediated by DLEU1 in GC was partly by regulating KLF2. Collectively, our findings manifested that DLEU1 might serve as an oncogene in GC. 

Retracted: No

PubPeer comments:
 In Figure 3E, part of the flow cytometry dot plots have been reused and presented as something else. This article figures as no. 2 in the Best of Cancer Gene Therapy 2018--2019 Collection. Congratulations! ![file] , 
 #1 Thank you very much for pointing this questions. As we are busy with the prevention and control of the recent 2019-nCoV, we did not deal with it in time. We have communicated with the editor of cancer gene therapyuff0c We will read the preliminary research records and checked them. , 
 Dear Indigofera Tanganyikensis: Thank you very much for pointing the problemuff0cWe have corrected it. https: rdcu.be cxzlM. Thank you again for your work. , 
 #3 Hello Yimin Song, Thanks for correcting! The erratum states that a  mistake occurred during image editing composition . Can you please elaborate on that? Flow cytometry plots showing a partial duplication of points between unrelated measurements are frequently flagged on PubPeer. Thus far no author has clarified the process that made that happen. What software do you use and how did (operating) that software cause the mix-up of different measurements? ,
hSirT1-dependent regulation of the PCAF-E2F1-p73 apoptotic pathway in response to DNA damage
Authors: Tiziana Bruno
Stefania Vossio
Laura Belloni
Valeria Schinzari
Cecilia Scisciani
Massimo Levrero
Maurizio Fanciulli
Francesca Guerrieri
Natalia Pediconi
Journal: Molecular and Cellular Biology (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: hSirT1; PCAF; E2F1; P1p73 promoter; apoptosis
Affiliations: Laboratory of Gene Expression, Fondazione A Cesalpino, Viale del Policlinico 155, 00161 Rome, Italy., INSERM U785/Sapienza Università, Viale del Policlinico 155, 00161 Rome, Italy, Department of Internal Medicine, Sapienza Università, Viale del Policlinico 155, 00161 Rome, Italy, Laboratory of Gene Expression, Fondazione A Cesalpino, Viale del Policlinico 155, 00161 Rome, Italy, Rome Oncogenomic Center, Regina Elena Cancer Institute, Via delle Messi d'Oro 156, 00158 Rome, Italy, Fondazione Cenci Bolognetti/Istituto Pasteur, Sapienza Università, Viale del Policlinico 155, 00161 Rome, Italy

Abstract:  The NAD(+)-dependent histone deacetylase hSirT1 regulates cell survival and stress responses by inhibiting p53-, NF-kappaB-, and E2F1-dependent transcription. Here we show that the hSirT1/PCAF interaction controls the E2F1/p73 apoptotic pathway. hSirT1 represses E2F1-dependent P1p73 promoter activity in untreated cells and inhibits its activation in response to DNA damage. hSirT1, PCAF, and E2F1 are corecruited in vivo on theP1p73 promoter. hSirT1 deacetylates PCAF in vitro and modulates PCAF acetylation in vivo. In cells exposed to apoptotic DNA damage, nuclear NAD(+) levels decrease and inactivate hSirT1 without altering the hSirT1 interaction with PCAF and hSirT1 binding to the P1p73 promoter. The reactivation of hSirT1 by pyruvate that increases the [NAD(+)]/[NADH] ratio completely abolished the DNA damage-induced activation of TAp73 expression, thus linking the modulation of chromatin-bound hSirT1 deacetylase activity by the intracellular redox state with P1p73 promoter activity. The release of PCAF from hSirT1 repression favors the assembly of transcriptionally active PCAF/E2F1 complexes onto the P1p73 promoter and p53-independent apoptosis. Our results identify hSirT1 and PCAF as potential targets to modulate tumor cell survival and chemoresistance irrespective of p53 status. 

Retracted: No

PubPeer comments:
 Figure 1C. * Blue boxes: Two panels look very similar, as also confirmed by false color versions. Figure 3C. * Red boxes: Two panels look very similar, as also confirmed by false color versions. ![file] Reported to the journal in September 2016. No action was taken. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
Gene loss and parallel evolution contribute to species difference in flower color
Authors: Stacey D Smith
Mark D Rausher
Journal: Molecular biology and evolution (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: regulatory evolution; gene copy number; anthocyanin pigment pathway; genetic changes; red flowers
Affiliations: Department of Biology, Duke University, USA. 

Abstract:  Although the importance of regulatory and functional sequence evolution in generating species differences has been studied to some extent, much less is known about the role of other types of genomic changes, such as fluctuation in gene copy number. Here, we apply analyses of gene function and expression of anthocyanin pigment pathway genes, as well as cosegregation analyses in backcross populations, to examine the genetic changes involved in the shift from blue to red flowers in Andean Iochroma (Solanaceae). We demonstrate that deletion of a gene coding for an anthocyanin pathway enzyme was necessary for the transition to red floral pigmentation. The downregulation of a second pathway gene was also necessary for the novel flower color, and this regulatory pattern parallels the genetic change in the two other red-flowered species in the sister family Convolvulaceae in which flower color change has been examined genetically. Finally, we document a shift in enzymatic function at a third locus, but the importance of this change in the transition to red flowers depends on the exact order with which the three changes occurred. This study shows that gene inactivation or loss can be involved in the origin of phenotypic differences between species, thereby restricting the possibility of reversion to the ancestral state. It also demonstrates that parallel evolution of red flowers in three different species occurs via a common developmental/regulatory change but by mutations in different genes. 

Retracted: No

PubPeer comments:
 Figure 7A appears to have one image that represents two different species: I. cyaneum and I. gesnerioides. Could the authors comment? *** ![file] , 
 I think this is fine. They are both F1s. The way the figure is composed with the black boxes could easily lead to this confusion though. ,
A Laboratory Approach on the Hybrid-Enhanced Oil Recovery Techniques with Different Saline Brines in Sandstone Reservoirs
Authors: Tomas Pieler
Annette Borchers
Journal: Processes (2020)
Discipline: CHEMISTRY
Keywords: Xenopus embryos; pluripotent cells; organogenesis; human embryonic stem cells; animal cap cells

Abstract:  Xenopus embryos provide a rich source of pluripotent cells that can be differentiated into functional organs. Since the molecular principles of vertebrate organogenesis appear to be conserved between Xenopus and mammals, this system can provide useful guidelines for the directional manipulation of human embryonic stem cells. Pluripotent Xenopus cells can be easily isolated from the animal pole of blastula stage Xenopus embryos. These so called "animal cap" cells represent prospective ectodermal cells, but give rise to endodermal, mesodermal and neuro-ectodermal derivatives if treated with the appropriate factors. These factors include evolutionary conserved modulators of the key developmental signal transduction pathways that can be supplied either by mRNA microinjection or direct application of recombinant proteins. This relatively simple system has added to our understanding of pancreas, liver, kidney, eye and heart development. In particular, recent studies have used animal cap cells to generate ectopic eyes and hearts, setting the stage for future work aimed at programming pluripotent cells for regenerative medicine. 

Retracted: No

PubPeer comments:
 Could the authors review Table 1 and 4 and confirm whether the apparent repetition of figures is due to samples C and D representing the same formulation or something else? *** ![file] ,
Comparison of real-time quantitative PCR and culture for the diagnosis of emerging Rickettsioses
Authors: Didier Raoult
Emmanouil Angelakis
Jean-Marc Rolain
Hervé Richet
Bernard La Scola
Journal: PLoS Neglected Tropical Diseases (2012)
Discipline: IMMUNOLOGY
Keywords: Rickettsia species; PCR; culture sensitivity; sampling delay; antibiotic treatment

Abstract:  Background: Isolation of Rickettsia species from skin biopsies may be replaced by PCR. We evaluated culture sensitivity compared to PCR based on sampling delay and previous antibiotic treatment. Methodology/principal findings: Skin biopsies and ticks from patients with suspected Rickettsia infection were screened for Rickettsia spp. using qPCR, and positive results were amplified and sequenced for the gltA and ompA genes. Immunofluorescence for spotted fever group rickettsial antigens was done for 79 patients. All skin biopsies and only ticks that tested positive using qPCR were cultured in human embryonic lung (HEL) fibroblasts using the centrifugation-shell vial technique. Patients and ticks were classified as definitely having rickettsioses if there was direct evidence of infection with a Rickettsia sp. using culture or molecular assays or in patients if serology was positive. Data on previous antibiotic treatments were obtained for patients with rickettsiosis. Rickettsia spp. infection was diagnosed in 47 out of 145 patients (32%), 41 by PCR and 12 by culture, whereas 3 isolates were obtained from PCR negative biopsies. For 3 of the patients serology was positive although PCR and culture were negative. Rickettsia africae was the most common detected species (n = 25, [17.2%]) and isolated bacterium (n = 5, [3.4%]). The probability of isolating Rickettsia spp. was 12 times higher in untreated patients and 5.4 times higher in patients from our hometown. Rickettsia spp. was amplified in 24 out of 95 ticks (25%) and we isolated 7 R. slovaca and 1 R. raoultii from Dermacentor marginatus. Conclusions/significance: We found a positive correlation between the bacteria copies and the isolation success in skin biopsies and ticks. Culture remains critical for strain analysis but is less sensitive than serology and PCR for the diagnosis of a Rickettsia infection. 

Retracted: No

PubPeer comments:
 The content of Figure 2 appears unrelated to the caption: ![file] The datasets listed in the caption are not presented in the figure. Also, the figure appears identical to Figure 1 in https: doi.org 10.4269 ajtmh.12-0212, where it represents something else entirely:  Figure 1. Comparison between cycle threshold (Ct) values and log10 values of the number (nb) of copies mL of the Coxiella burnetii IS1111 spacer region, France. I was made aware of this figure on Twitter: https: twitter.com TatayoyoKesski1 status 1372874643254743040 ,
mTOR-dependent suppression of protein phosphatase 2A is critical for phospholipase D survival signals in human breast cancer cells
Authors: Stefan Knirr
Rafal M Pielak
David A Foster
Yang Zheng
Vanessa Rodrik
Li Hui
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: tumor progression; survival signals; phospholipase D activity; breast cancer; protein phosphatase 2A
Affiliations: Department of Biological Sciences, Hunter College of the City University of New York, New York, New York 10021, USA.

Abstract:  A critical aspect of tumor progression is the generation of survival signals that overcome default apoptotic programs. Recent studies have revealed that elevated phospholipase D activity generates survival signals in breast and perhaps other human cancers. We report here that the elevated phospholipase D activity in the human breast cancer cell line MDA-MB-231 suppresses the activity of the putative tumor suppressor protein phosphatase 2A in a mammalian target of rapamycin (mTOR)-dependent manner. Increasing the phospholipase D activity in MCF7 cells also suppressed protein phosphatase 2A activity. Elevated phospholipase D activity suppressed association of protein phosphatase 2A with both ribosomal subunit S6-kinase and eukaryotic initiation factor 4E-binding protein 1. Suppression of protein phosphatase 2A by SV40 small t-antigen has been reported to be critical for the transformation of human cells with SV40 early region genes. Consistent with a critical role for protein phosphatase 2A in phospholipase D survival signals, either SV40 small t-antigen or pharmacological suppression of protein phosphatase 2A restored survival signals lost by the suppression of either phospholipase D or mTOR. Blocking phospholipase D signals also led to reduced phosphorylation of the pro-apoptotic protein BAD at the protein phosphatase 2A dephosphorylation site at Ser-112. The ability of phospholipase D to suppress protein phosphatase 2A identifies a critical target of an emerging phospholipase D/mTOR survival pathway in the transformation of human cells. 

Retracted: No

PubPeer comments:
 Figure 1 u2013 more similar than expected ![file] ![file] Figure 2: more similar than expected ![file] ,
Cyclic AMP-dependent protein lysine acylation in mycobacteria regulates fatty acid and propionate metabolism
Authors: Ann Terene Thomas
Subhalaxmi Nambi
Sandhya S Visweswariah
Moitrayee Bhattacharyya
Vaishnavi Ravikumar
Kallol Gupta
Parvathy Ramakrishnan
Nida Siddiqui
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Acetyl Coenzyme A; Actinobacteria; Fatty Acid Metabolism; Mass Spectrometry (MS); Mycobacteria

Abstract:  Acetylation of lysine residues is a posttranslational modification that is used by both eukaryotes and prokaryotes to regulate a variety of biological processes. Here we identify multiple substrates for the cAMP-dependent protein lysine acetyltransferase from Mycobacterium tuberculosis (KATmt). We demonstrate that a catalytically important lysine residue in a number of FadD (fatty acyl CoA synthetase) enzymes is acetylated by KATmt in a cAMP-dependent manner and that acetylation inhibits the activity of FadD enzymes. A sirtuin-like enzyme can deacetylate multiple FadDs, thus completing the regulatory cycle. Using a strain deleted for the KATmt ortholog in Mycobacterium bovis Bacillus Calmette-Guérin (BCG), we show for the first time that acetylation is dependent on intracellular cAMP levels. KATmt can utilize propionyl CoA as a substrate and, therefore, plays a critical role in alleviating propionyl CoA toxicity in mycobacteria by inactivating acyl CoA synthetase (ACS). The precision by which mycobacteria can regulate the metabolism of fatty acids in a cAMP-dependent manner appears to be unparalleled in other biological organisms and is ideally suited to adapt to the complex environment that pathogenic mycobacteria experience in the host. 

Retracted: No

PubPeer comments:
 ![file] , 
 Thank you for your comment. Yes indeed, the figures are the same and this error has arisen during the compilation of the final version of the paper. I am attaching the correct figure and will also inform the journal so than an Addendum can be made to the paper. [file] , 
 J Biol Chem will publish the following correction An incorrect image was published for Fig 5A which did not match the version that was published as a Paper in Press on April 3, 2013. This error has now been correct and does not affect the results or conclusions of this work. ,