syedzayyan/paper_mill_benchmark huggingface dataset:
LncRNA ATB promotes proliferation and metastasis in A549 cells by downregulation of microRNA‐494

Lung cancer is a commonly diagnosed disease with poor prognosis.Novel therapeutic targets and deep understanding of the regulatory mechanisms in lung cancer are of great importance.We aimed to figure out the functional roles of lnc rna‐activated by transforming growth factor‐β (atb) in a549 cells as well as the underlying molecular mechanisms.Atb was non‐physiologically expressed in a549 cells after cell transfection.Then, cell proliferation, expressions of proteins related to proliferation and epithelial‐mesenchymal transition (emt), migration, and invasion were measured by brd u incorporation assay, western blot analysis, and transwell assay, respectively.Afterwards, mi r‐494 expression in transfected a549 cells was determined by quantitative reverse transcription pcr.Meanwhile, effects of mi r‐494 overexpression on atb‐overexpressed cells were assessed.Finally, the phosphorylation levels of akt and key kinases in the janus‐activated kinase (jak)/signal transducer and activator of transcription‐3 (stat3) pathway were detected by western blot analysis.Atb overexpression promoted proliferation, migration, and invasion of a549 cells.Meanwhile, emt of a549 cells was also enhanced.Atb silence showed the opposite influence.Expression of mi r‐494 was negatively regulated by atb.Following experiments showed atb‐induced alterations of proliferation, migration, invasion, and emt were all reversed by mi r‐494 overexpression.Finally, we proved that atb increased phosphorylated levels of akt, jak1, and stat3, and those increases were all reversed by mi r‐494 overexpression.We interestingly figured out that atb promoted proliferation, migration, invasion, and emt through down‐regulating mi r‐494 in a549 cells.Moreover, atb might activate akt and the jak/stat3 pathway via down‐regulating mi r‐494.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Euxanthone inhibits glycolysis and triggers mitochondria-mediated apoptosis by targeting

Epithelial ovarian cancer (eoc) is one of the most prevalent gynaecological cancers.Euxanthone, an active ingredient of the medicinal plant polygala caudata , exhibits a selective cytotoxic effect in tumour cells.The present study was aimed to determine whether euxanthone could suppress ovarian tumour growth, and to study the relevant mechanism.Two eoc cell lines, skov3 and a2780, were used as the in vitro model and treated with euxanthone.Cell viability and apoptosis were assayed using cell counting kit‐8 (cck‐8) and annexin‐v fitc/pi staining, respectively.Commercially available kits were used to measure the glucose consumption, lactate production, and intracellular atp levels.Western blots assay was conducted to examine the level of apoptotic markers.To examine the roles of hk2 and stat3 in the anti‐tumour effect of euxanthone, cells were transfected with vectors overexpressing hk2 or stat3, and assayed as above.Finally, skov3 cells were injected to mice models to appreciate the anti‐neoplastic effect of euxanthone in vivo.We found that euxanthone impaired the cell viability and induced apoptosis via the intrinsic pathway in a concentration‐dependent fashion in both skov3 and a2780 cells.Euxanthone also caused inhibition of glycolysis.Apoptosis and glycolysis inhibition was mediated by the downregulation of hk2, which in turn was a result of stat3 inactivation.In vivo experiments also supported that euxanthone could exert anti‐cancer activities without general toxicity.In conclusion, euxanthone triggered mitochondrial apoptosis and inhibited glycolysis in eoc cells.Significance of the study euxanthone triggered mitochondrial apoptosis and inhibited glycolysis in eoc cells.Our findings provide preliminary experimental data that support further studies on the potential therapeutic role of euxanthone in ovarian cancer.

Journal: Cell Biochemistry and Function (2018)
Publication types: Research Article;
S100A9 gene silencing inhibits the release of pro‐inflammatory cytokines by blocking the IL‐17 signalling pathway in mice with acute pancreatitis

The study aimed to investigate whether s100a9 gene silencing mediating the il ‐17 pathway affected the release of pro‐inflammatory cytokines in acute pancreatitis ( ap ).Kunming mice were assigned to the normal, ap , ap + negative control ( nc ), ap + sh rna , ap + ig g and ap + anti il ‐17 groups.Elisa was applied to measure expressions of amy , ldh , crp , tnf ‐α, il ‐6 and il ‐8.The cells were distributed into the control, blank, nc , sh rna 1 and sh rna 2 groups.Mtt assay, flow cytometry, rt ‐ q pcr and western blotting were used to evaluate cell proliferation, cell cycle and apoptosis, and expressions of s100a9, tlr 4, rage , il ‐17, hmgb 1 and s100a12 in tissues and cells.Compared with the normal group, the ap group displayed increased expressions of amy , ldh , crp , tnf α, il ‐6, il ‐8, s100a9, tlr 4, rage , il ‐17, hmgb 1 and s100a12.The ap + sh rna and ap + anti il ‐17 groups exhibited an opposite trend.The in vivo results: compare with the control group, the blank, nc , sh rna 1 and sh rna 2 groups demonstrated increased expressions of s100a9, tlr 4, rage , il ‐17, hmgb 1 and s100a12, as well as cell apoptosis and cells at the g1 phase, with reduced proliferation.Compared with the blank and nc groups, the sh rna 1 and sh rna 2 groups had declined expressions of s100a9, tlr 4, rage , il ‐17, hmgb 1 and s100a12, as well as cell apoptosis and cells at the g1 phase, with elevated proliferation.The results indicated that s100a9 gene silencing suppressed the release of pro‐inflammatory cytokines through blocking of the il ‐17 pathway in ap .

Journal: Journal of Cellular and Molecular Medicine (JCMM) (2018)
Publication types: Research Article;
Immunoregulatory Role of MicroRNA-21 in Macrophages in Response to Bacillus Calmette- Guerin Infection Involves Modulation of the TLR4/MyD88 Signaling Pathway

The purpose of this study is to explore the immunoregulatory role of micro rna-21 (mi r-21) targeting of the tlr4/my d88 signaling pathway in macrophages in response to bacillus calmette-guerin (bcg) infection.Methods: after infection with bcg, mouse raw246.7 cells were assigned into control, bcg, mi r-21 mimic + bcg, mimic-negative control (nc) + bcg, mi r-21 inhibitor + bcg, inhibitor-nc + bcg, bcg + tak242 (an inhibitor of the tlr4 signaling pathway), and mi r-21 inhibitor + tak242 + bcg groups.Western blotting and q rt-pcr were used to detect the expression of mi r-21, tlr4 and my d88.The levels of tnf-a, il-6 and il-10 were detected by enzyme-linked immunosorbent assay (elisa).Cell viability was measured using an mtt assay.Cell apoptosis and necrosis rates were detected using flow cytometry.Results: compared with the control group, mi r-21 expression and levels of tnf-a, il-6 and il-10, as well as cell apoptosis and necrosis rates, were elevated, while expression of tlr4 and my d88, as well as cell viability, were reduced in bcg infection groups.Compared with the bcg group, mi r-21 expression was increased in the mi r-21 mimic + bcg group but decreased in the mi r-21 inhibitor + bcg and mi r-21 inhibitor + tak242 + bcg groups.The expression of tlr4 and my d88, as well as the cell viability, were decreased, while levels of tnf-a, il-6 and il-10, as well as cell apoptosis and necrosis rates, were increased in the mi r-21 mimic + bcg and tak242 + bcg groups.The opposite trends were found in the mi r-21 inhibitor + bcg group.Compared with the tak242 + bcg group, the mi r-21 inhibitor + tak242 + bcg group had higher expression of tlr4 and my d88 as well as higher cell viability and lower levels of tnf-a, il-6, il-10, cell apoptosis and necrosis rates.However, the mi r-21 inhibitor + tak242 + bcg group exhibited the opposite trends when compared with the mi r-21 inhibitor + bcg group.Conclusion: our results suggest that mi r-21 can negatively modulate the tlr4/my d88 signaling pathway, resulting in decreased cell viability, increased cell apoptosis and increased levels of inflammatory factors following bcg infection in macrophages.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
Effects of Fibronectin 1 on Cell Proliferation, Senescence and Apoptosis of Human Glioma Cells Through the PI3K/AKT Signaling Pathway

The current study aimed to investigate the role by which fibronectin 1 (fn1) influences the cell cycle, senescence and apoptosis in human glioma cells through the pi3k/ akt signaling pathway.Methods: differentially expressed genes (degs) were identified based on gene expression data (gse12657, gse15824 and gse45921 datasets) and probe annotation files from gene expression omnibus.The degs were identified in connection with gene ontology (go) enrichment analysis and with the kyoto encyclopedia of genes and genomes (kegg) pathway enrichment analysis.The positive expression of the fn1 protein was detected by immunohistochemistry.The glioma cell lines u251 and t98g were selected and assigned into blank, negative control (nc) and si rna-fn1 groups.A dual luciferase reporter gene assay was used to investigate the effects of fn1 on transcriptional activity through the pi3k/akt signaling pathway.An mtt assay was applied for the detection of cell proliferation, while flow cytometry was employed for cell cycle stage and cellular apoptosis detection.Β-galactosidase staining was utilized to detect cellular senescence, a scratch test was applied to evaluate cell migration, and a transwell assay was used to analyze cell invasion.Western blotting and q rt-pcr methods were used to detect the protein and m rna expression levels, respectively, of the fn1 gene and the related genes in the pi3k/akt pathway (pi3k, akt and pten), the cell cycle (p rb, cdk4 and cyclin d1) and cell senescence (p16 and p21) among the collected tissues and cells.Results: gse12657 profiling revealed fn1 to be the most upregulated gene in glioma.Regarding the gse12657 and gse15824 datasets, fn1 gene expression was higher in glioma tissues than in normal tissues.Go enrichment analysis and kegg pathway enrichment analysis indicated that fn1 is involved in the synthesis of extracellular matrix (ecm) components and the pi3k/akt signaling pathway.Verification was provided, indicating the role played by the fn1 gene in the regulation of the pi3k/akt signaling pathway, as silencing the fn1 gene was found to inhibit cell proliferation, promote cell apoptosis and senescence, and reduce migration and invasion through the down-regulation of fn1 gene expression and disruption of the pi3k-akt signaling pathway.Conclusion: the findings of this study provide evidence highlighting the prominent role played by fn1 in stimulating glioma growth, invasion, and survival through the activation of the pi3k/akt signaling pathway.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Physcion8-O-Β-Glucopyranoside Alleviates Oxidized Low-Density Lipoprotein-Induced Human Umbilical Vein Endothelial Cells Injury by Inducing Autophagy Via AMPK/SIRT1 Signaling

Vascular endothelial cell dysfunction plays a crucial role in the initiation and development of atherosclerosis.Physcion 8-o-β-glucopyranoside (pg), an anthraquinone extracted from polygonum cuspidatum , has a number of pharmacological functions.The aim of this study was to elucidate the protective effects of pg against oxidized low-density lipoprotein (ox-ldl) in vecs.Methods and materials: human umbilical vein endothelial cells (huvecs) were used as the in vitro model.Cell viability and apoptosis were, respectively, assessed by cck-8 assay and annexin-v/pi staining.Formation of autophagosomes was visualized by acridine orange staining, and the autophagy flux was tracked after infecting the cells with the m rfp-gfp-lc3 adenovirus.The expression levels of various apoptosis and autophagy-associated marker proteins were detected by western blotting.Results: pretreatment with pg protected the huvecs from ox-ldl–induced apoptosis.In addition, pg promoted autophagy in huvecs, which was responsible for its antiapoptotic effects.Finally, activation of ampk/sirt1 signaling was upstream of pg-induced autophagy.Conclusions: pg has potential pharmacological effects against oxidative damage–induced huvec injury through inducing ampk/sirt1-mediated autophagy.

Journal: Journal of Cardiovascular Pharmacology (2019)
Publication types: Research Article;
Downregulation of long noncoding RNA Sox2ot protects PC‐12 cells from hydrogen peroxide–induced injury in spinal cord injury via regulating the miR‐211‐myeloid cell leukemia‐1 isoform2 axis

This study aimed to investigate the effects and possible mechanisms of long noncoding rna (lnc rna) sox2 overlapping transcript (sox2ot) on hydrogen peroxide (h 2 o 2 )‐induced injury in pheochromocytoma (pc‐12) cells.Pc‐12 cells were treated with h 2 o 2 to cell injury.The cells were transfected with short‐hairpin rna directed against sox2ot (sh‐sox2ot), small interfering rna directed against myeloid cell leukemia‐1 (mcl‐1) isoform2 (si‐mcl‐1), a mi r‐211 mimic, a mi r‐211 inhibitor, and their negative controls.Under different transfected treatments, cell viability, migration, invasion, and apoptosis as well as the expressions of apoptosis‐ and autophagy‐related proteins were investigated.Besides, the regulatory relationships between sox2ot and mi r‐211, mi r‐211 and mcl‐1, as well as between mcl‐1 and the protein kinase b (akt)/mammalian target of the rapamycin (m tor)/p70 ribosomal s6 protein kinase (p70s6k) signaling pathway were explored.Suppression of sox2ot inhibited h 2 o 2 ‐induced pc‐12 cell injury by increasing cell viability, migration, invasion, and decreasing apoptosis and autophagy.Moreover, suppression of sox2ot increased mi r‐211 expression and alleviated h 2 o 2 ‐induced injury in pc‐12 cells possibly via upregulation of mi r‐211.Furthermore, mcl‐1 isoform2 was identified as a direct target of mi r‐211 and could be negatively regulated by mi r‐211.Suppression of mi r‐211 aggravated h 2 o 2 ‐induced cell injury by regulation of mcl‐1 isoform2.Besides, inhibition of mi r‐211 suppressed the activation of the akt/m tor/p70s6k signaling pathway in h 2 o 2 ‐treated pc‐12 cells, which was reversed after knockdown of mcl‐1 isoform2 at the same time.Our findings indicate that downregulation of sox2ot may protect pc‐12 cells from h 2 o 2 ‐induced injury in sci via targeting the mi r‐211/mcl‐1 isoform2 axis.Mcl‐1 isoform2 may further regulate the activation of the akt/m tor/p70s6k pathway to mediate h 2 o 2 ‐induced injury.The sox2ot‐mi r‐211‐mcl‐1 isoform2 axis may be a promising therapeutic strategy for sci.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
ZIC2 promotes viability and invasion of human osteosarcoma cells by suppressing SHIP2 expression and activating PI3K/AKT pathways

Osteosarcoma is a malignant tumor of the skeletal system.The zinc finger transcription factor zic2 has been reported to be highly expressed in human cancers.The present study evaluated the effects of zic2 and the possible underlying mechanisms in the human osteosarcoma cells.The expression levels of zic2 in human fetal osteoblastic cell line (h fob1.19), osteosarcoma cell lines (u‐2os, sao s2, and mg63), normal bone tissue, and osteosarcoma tumor were analyzed by western blot, and real‐time quantitative rt‐pcr (q rt‐pcr).Osteosarcoma cells with either overexpressed zic2 or suppressed zic2 were analyzed to determine cell viability, colony formation, and cell invasion.The expressions of ship2 and pi3k/akt signal pathway‐related proteins were analyzed by western blot and q rt‐pcr.We first showed that zic2 is highly expressed in osteosarcoma cells and tissues.Then we demonstrated that overexpression of zic2 promoted viability, migration, and invasion of osteosarcoma cells, whereas suppression of zic2 showed opposite effects.Furthermore, ship2 expression was negatively regulated by zic2.Importantly, zic2 overexpression activated the pi3k/akt signal pathway; however, overexpressed ship2 inhibited these effects.Lastly, we showed that activation of the pi3k/akt signal pathway is essential for the effects of zic2 on osteosarcoma cells, as the effects of zic2 on the osteosarcoma cells were reversed by a pi3k/akt inhibitor.Overall, zic2 is highly expressed in osteosarcoma cells and tissues, and its overexpression promotes viability, invasion of osteosarcoma cells via ship2 suppression, and pi3k/akt activation.Thus, zic2 can be considered as a novel drug target for osteosarcoma management.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Long noncoding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis

This study aimed to elucidate the roles of long non‐coding rna snhg14 in gastric cancer development.Lnc rna snhg14 was markedly up‐regulated in gastric cancer tissues and cells.Knockdown of snhg14 significantly inhibited sgc‐7901 cell viability, migration, invasion, and promoted cell apoptosis.In addition, mi r‐145 was negatively regulated by snhg14 and the effects of snhg14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis‐related proteins and emt‐markers were reversed by inhibition of mi r‐145 at the same time.Furthermore, sox9 was verified as a functional target of mi r‐145, and mi r‐145 regulated tumor malignant behaviors through regulating sox9.Besides, knockdown of snhg14 inhibited the expression of p‐pi3 k, p‐akt, and p‐m tor and promoted pten expression, where mi r‐145 inhibition had opposite effects.Moreover, the activated pi3 k/akt/m tor pathway caused by mi r‐145 inhibition was counteracted after knockdown of sox9.Our findings indicate that up‐regulation of lnc rna snhg14 may contribute to gastric cancer development via targeting mi r‐145/sox9 axis and involving in pi3 k/akt/m tor pathway.Snhg14‐mi r‐145/sox9 axis may be a promising therapeutic strategy for gastric cancer treatment.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Negative feedback of NF-κB signaling by long noncoding RNA MALAT1 controls lipopolysaccharide-induced inflammation injury in human lung fibroblasts WI-38

The study was designed to elucidate the regulatory mechanism of long noncoding rna human metastasis associated lung adenocarcinoma transcript 1 (malat1) in lipopolysaccharides (lps)‐caused inflammation injury in human lung fibroblasts wi‐38.Wi‐38 cells were stimulated with lps to construct acute pneumonia cell model.Malat1 in lps‐stimulated wi‐38 cells was examined.Lps‐induced inflammation injury was estimated using viability, apoptosis, and cytokine secretion including interleukin‐1β (il‐1β) and il‐6.Furthermore, the modulatory relations of malat1 and nuclear factor‐kappa b (nf‐κb) signaling were explored.We found that the sensitivity of wi‐38 cells to apoptosis was enhanced by lps‐caused inflammation.Moreover, lps promoted malat1 expression which was found to alleviate lps‐caused damages.Besides, nf‐κb p65 overexpression resulted in an increased expression of malat1, and malat1 was identified as a target gene of p65.Furthermore, overexpression of malat1 reduced nf‐κb activation.Pulldown assay showed that malat1 could directly interact with p65.Taken together, our findings revealed that malat1 was upregulated in lps‐stimulated wi‐38 cells.Through directly interacting with p65, malat1 blocked lps‐caused activation of nf‐κb and repressed lps‐induced inflammation injury.Malat1 may serve as a potential diagnostic indicator or therapeutic target for pneumonia.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Dexmedetomidine Inhibits Osteosarcoma Cell Proliferation and Migration, and Promotes Apoptosis by Regulating miR-520a-3p

This study aimed to investigate the effect of dexmedetomidine (dex) on osteosarcoma (os) cell line mg63 and to explore the possible relationship between dex and mi r-520-3p in os.The results showed that dex could upregulate mi r-520-3p, which directly targeted akt1 .Additionally, mi r-520-3p also inhibited mg63 cell proliferation and migration, promoted apoptosis, and suppressed protein expressions of akt, p-akt, p-m tor, and p-erk1/2.Dex can inhibit os cell proliferation and migration and promote apoptosis by upregulating the expression level of mi r-520a-3p.Dex may serve as a potential therapeutic agent in os treatment, and mi r-520a-3p may be a potential target in the therapy of os.

Journal: Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics (2018)
Publication types: Research Article;
Physcion 8‐O‐β‐glucopyranoside inhibits testicular germ cell tumors through regulating microRNA‐199a

“ physcion 8 ‐ o ‐ β ‐ glucopyranoside inhibits testicular germ cell tumors through regulating micro rna ‐ 199a ”, by xiangyang dou, meihua wang, tao zhang, jiapei yao.The above article, published in the anatomical record on early view on wiley online library on 04/dec/2019 ( ) is retracted by agreement among the authors and the editor‐in‐chief, dr.Kurt h.Albertine, with notification to the american association for anatomy and wiley periodicals llc.The decision is the result of an investigation that revealed issues of scientific integrity in the data that compromise the findings of the paper.

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2019)
Publication types: Research Article;
Alpinumisoflavone Inhibits Tumor Growth and Metastasis in Papillary Thyroid Cancer via Upregulating miR‐141‐3p

Alpinumisoflavone (aif) as a principal active ingredient of traditional chinese herb derris eriocarpa exerts a broad spectrum of anticancer activities against solid tumors.However, little is known about the effect of aif on papillary thyroid cancer (ptc).Objectives of this study are to investigate the effect of aif on cell growth, apoptosis, and metastasis of ptc cells and uncover its underlying mechanisms.Results showed that aif treatment notably suppressed cell viability, migration, invasion, and epithelial–mesenchymal transition (emt) process, as well as induced apoptotic cell death.In addition, microarray analysis results revealed that mi r‐141‐3p level was dramatically elevated upon aif insulation, suggesting that mi r‐141‐3p may mediate the suppressive role of aif against ptc.Moreover, mi r‐141‐3p knockdown effectively reversed the effects of aif on cell growth, migration, invasion, and emt, while promoted ptc cell apoptosis escape.Furthermore, in vivo findings also confirmed that the antigrowth and antimetastasis activities of aif were, at least partly, mediated by upregulation of mi r‐141‐3p.Overall, aif could serve as a potential anticancer compound for ptc treatment.Anat rec, 2019.© 2019 american association for anatomy anat rec, 303:1842–1850, 2020.© 2019 american association for anatomy

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2019)
Publication types: Research Article;
Alpinumisoflavone exhibits anticancer activities in glioblastoma multiforme by suppressing glycolysis

“alpinumisoflavone exhibits anticancer activities in glioblastoma multiforme by suppressing glycolysis” by xingzhi zhao, ting zhang, kewei jiang, and henggao gao.The above article, published in the anatomical record on early view on wiley online library on 24/aug/2019 ( ) is retracted by agreement among the authors and the editor‐in‐chief, dr.Kurt h.Albertine, with notification to the american association for anatomy and wiley periodicals llc.The decision is the result of an investigation that revealed issues of scientific integrity in the data that compromise the findings of the paper

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2019)
Publication types: Research Article;