syedzayyan/paper_mill_benchmark huggingface dataset:
Suppression of microRNA-135b-5p protects against myocardial ischemia/reperfusion injury by activating JAK2/STAT3 signaling pathway in mice during sevoflurane anesthesia

The study aims to explore the effects of mi r-135b-5p on myocardial ischemia/reperfusion (i/r) injuries by regulating janus protein tyrosine kinase 2 (jak2)/signal transducer and activator of transcription (stat) signaling pathway by mediating inhalation anesthesia with sevoflurane.A sum of 120 healthy wistar male mice was assigned into six groups.Left ventricular ejection fraction (lvef) and left ventricular shortening fraction (lvsf) were detected.Cardiomyocyte apoptosis was determined by terminal dexynucleotidyl transferase mediated d utp-biotin nick end labeling (tunel) assay.Mi r-135b-5p expression, m rna and protein expression of p-stat3, p-jak2, stat3, jak2, b-cell lymphoma-2 (bcl-2) and bcl-2 associated x protein b (bax) were detected by quantitative real-time pcr (q rt-pcr) and western blotting.Target relationship between mi r-135b-5p and jak2 was confirmed by dual-luciferase reporter assay.The other five groups exhibited increased cardiomyocyte necrosis, apoptosis, mi r-135b-5p and bax expression, m rna expression of jak2 and stat3, and protein expression of p-stat3 and p-jak2 compared with the sham group, but showed decreased lvef, lvfs, and bcl-2 expression.Compared with the model and ag490 + sevo groups, the sevo, inhibitor + sevo and inhibitor + ag490 + sevo groups displayed reduced cardiomyocyte necrosis, apoptosis, mi r-135b-5p and bax expression, but displayed elevated m rna expression of jak2 and stat3, protein expression of p-stat3 and p-jak2, lvef, lvfs and bcl-2 expression.Compared with the sevo and inhibitor + ag490 + sevo groups, the ag490 + sevo group showed decreased lvef, lvfs, bcl-2 expression, m rna expressions of jak2 and stat3, and protein expressions of p-stat3 and p-jak2, but increased cardiomyocyte necrosis, apoptosis, and bax expressions.Mi r-135b-5p negatively targetted jak2.Inhibition of mi r-135b-5p can protect against myocardial i/r injury by activating jak2/stat3 signaling pathway through mediation of inhalation anesthesia with sevoflurane.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
Effects of microRNA-146a on the proliferation and apoptosis of human osteoarthritis chondrocytes by targeting TRAF6 through the NF-κB signaling pathway

The present study aims to investigate the effects of mi r-146a on the proliferation and apoptosis of human osteoarthritis (oa) chondrocytes by targeting tumour necrosis factor receptor-associated factor 6 (traf6) through nuclear factor-κb (nf-κb) signalling pathway.Human normal and oa chondrocytes were selected and divided into the normal group, blank group, negative control (nc) group, mi r-146a mimics group, mi r-146a inhibitors, mi r-146a inhibitor + si-traf6 group and si-traf6 group.Quantitative real-time pcr (q rt-pcr) was applied to detect the expressions of mi r-146a, traf6 m rna and nf-κb m rna.Western blotting was used to detect the protein expressions of traf6 and nf-κb.Cck-8 assay and flow cytometry were used to detect cell proliferation and apoptosis.Compared with normal chondrocytes, the expression of mi r-146a decreased, while the m rna and protein expressions of traf6 and nf-κb increased in oa chondrocytes.Oa chondrocytes had a lower proliferation rate and a higher apoptosis rate than the normal chondrocytes.Compared with the blank, nc and si-traf6 groups, the expression of mi r-146a increased in the mi r-146a mimics group, but decreased in the mi r-146a inhibitors and mi r-146a inhibitor + si-traf6 groups.Compared with the blank, nc and mi r-146a inhibitor + si-traf6 groups, the m rna and protein expressions of traf6 and nf-κb decreased, cell proliferation rate increased and cell apoptosis rate decreased in the mi r-146a mimics and si-traf6 groups, while opposite trends were observed in the mi r-146a inhibitors group.Our study suggests that mi r-146a could promote proliferation and inhibit apoptosis of oa chondrocytes by inhibiting traf6 expression and suppressing the activation of nf-κb signalling pathway.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
Circular RNA circFNDC3B protects renal carcinoma by miR-99a downregulation

Various circular rnas (circ rnas) have been reported to involve in carcinoma.This study explored the role and mechanism of circ rna circ fndc3b (circ fndc3b) in renal carcinoma (rc).The detection indicators in this paper were viability, colony, and migration, which respectively investigated by cell counting kit‐8, colony formation, and migration assay.Reverse transcriptase quantitative polymerase chain reaction tested and cell transfection changed circ fndc3b and mi r‐99a expression.Moreover, western blot tested relate‐proteins of proliferation, migration, and cell pathways were examined by western blot.Circ fndc3b was upregulated at rc tissues.Circ fndc3b enhanced cell viability, colony and migration, and mi r‐99a mimic played reverse impacts.Furthermore, circ fndc3b negatively regulated mi r‐99aand circ fndc3b restrained the janus kinase 1/signal transducer and activator of transcription 3 (jak1/stat3) and extracellular signal‐regulated kinase (erk) kinase (mek)/erk pathways by mi r‐99a downregulation.Overexpression of circ fndc3b enhanced cell viability, colony formation and migration by mi r‐99a downregulation via jak1/stat3 and mek/erk pathways.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
HOTAIR regulates lipopolysaccharide-induced inflammatory response in hepatocytes

It has been widely accepted that long‐noncoding rna (lnc rna) hox transcript antisense intergenic rna (hotair) emerges as a crucial mediator in inflammation.Here, we first detected hotair in lipopolysaccharide (lps)‐treated normal human liver cell line (l02) and hepatocellular carcinoma cell lines (c3a, hep g2, and smmc‐7721).Further, we explored the biological function of hotair in lps‐induced hepatocytes (l02 and c3a) lesions and investigated the molecular mechanisms.Besides, we focused on inflammatory signaling crosstalk.The inflammatory insults were assayed by cell counting kit‐8 (cck‐8), cell cycle and apoptosis analysis kit, and immunoblotting assay.Hotair level was examined by reverse‐transcription polymerase chain reaction.To determine the effect of hotair silence or overexpression in inflammation, we applied quantitative reverse‐transcription polymerase chain reaction, immunoblotting assay, and enzyme‐linked immuno sorbent assay.Regulator inhibitors of janus kinase/signal transducer and activator of transcription (jak2/stat3; ag490) and nuclear factor κb (nf‐κb; bay‐11–7082) were applied to treat cells.Our results suggested that lps induced the overexpression of hotair in l02, c3a, hep g2, and smmc‐7721 cells.Lps repressed viability, induced apoptosis, and facilitated the expression of interleukin (il)‐1β, il‐6, and tumor necrosis factor (tnf)‐α in l02 and c3a cells.Il‐1β, il‐6, and tnf‐α were upregulated by hotair overexpression while downregulated by hotair knockdown in lps‐treated cells.We further observed that hotair overexpression accelerated lps‐induced phosphorylation whereas hotair silence blocked this progress.Inhibition of jak/stat and nf‐κb contributed to the suppression of cytokines which was evoked by lps.Collectively, our findings indicated that hotair exerted a crucial role in cytokines expression by activating jak/stat and nf‐κb.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
Circular RNA circC3P1 restrains kidney cancer cell activity by regulating miR-21/PTEN axis and inactivating PI3K/AKT and NF- kB pathways

Kidney cancer (kc) seriously impacts public health.We detected the function and mechanism of circular rna c3p1 (circ c3p1) in kc cells.Cck‐8, flow cytometry, migration, and invasion assay were respectively used to investigate the efficacies of circ c3p1 and micro rna (mi r)‐21 on cell viability, apoptosis, migration, and invasion.Phosphatase and tensin homologue deleted on chromosome 10 (pten), circ c3p1, and mi r‐21 expression were changed by cell transfection and detected by quantitative reverse‐transcription polymerase chain reaction.Moreover, the apoptosis/pathways‐related proteins and proteins were detected by western blot analysis.Besides, the relation between pten and mi r‐21 was detected by luciferase assay.Circ c3p1 and pten were downregulated while mi r‐21 was upregulated in kc tissues.Circ c3p1 declined cell viability, migration, and invasion and caused apoptosis.Furthermore, circ c3p1 negatively regulated mi r‐21; mi r‐21 mimic could reverse the efficacies of circ c3p1.Besides, circ c3p1 restrained the pi3k/akt and nf‐κb pathways by downregulating mi r‐21.Finally, pten was authenticated as a target of mi r‐21.Circ c3p1 restrained kc cell growth, migration, and invasion by regulating mi r‐21/pten axis and inactivating pi3k/akt and nf‐κb signaling pathways.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
K-Ras-PI3K regulates H3K56ac through PCAF to elevate the occurrence and growth of liver cancer

H3 modification is related to a wide range of tumors, including liver cancer.The ras passageway is actuated in human diseases.Thus, we investigated the roles of ras in liver cancer cells via acetylation of h3k56.Ras‐carrying g12v and y40c site mutation was transfected into liver cancer cell lines snu‐475 and sk‐hep‐1.Acetylation of h3k56 and phosphatidylinositol 3‐kinase (pi3k), p300/cbp‐associated factor (pcaf) and mouse double minute 2 homolog (mdm2) was tested via western blot.Cell activity, colonies, and migration were tested via cell counting kit‐8, soft‐agar colony formation, and transwell experiment, respectively.Sirtuin 6 (sirt6) and pcaf were tested via quantitative reverse transcription polymerase chain reaction (q rt‐pcr).Chromatin immunoprecipitation was employed to test the relationship between ras and downstream elements.Flow cytometry was employed to test cell cycle series.We found that ras g12v/y40c transfection reduced the acetylation of h3k56 and activated phosphorylation of protein kinase b.H3k56q (h3k56ac overexpression) suppressed cell activity, colonies, and migration.H3k56ac changed ras downstream factors expression.Ras g12v/y40c bound to ras‐pi3k downstream elements' promoters.Sirt6 silencing raised h3k56ac and suppressed cell activity, migration and s phage cell percentage.Sirt6 silence transformed expression of downstream elements.Pcaf and h3k56ac demonstrated the close current while mdm2 was conversed.In summary, the ras‐pi3k passageway promoted cell growth and metastasis via decreasing h3k56ac, in which mdm2‐mediated pcaf was involved.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
Propofol exerts anticancer activity on hepatocellular carcinoma cells by raising lncRNA DGCR5

Hepatocellular carcinoma is one of the most fatal cancers worldwide.Propofol is an intravenous anesthetic extensively used in clinical.Herein, we tested the anticancer activity of propofol on hepatocellular carcinoma, along with the internal molecular mechanism related to lnc rna di george syndrome critical region gene 5 (dgcr5).Followed by propofol stimulation, hepatocellular carcinoma huh‐7 and hep g2 cell viability, proliferation, migration, invasion, and apoptosis were tested, respectively.Then, dgcr5 expression levels in hepatocellular carcinoma tissues and cells were measured.Sh‐dgcr5 was transfected to silence dgcr5 expression.Subsequently, the influence of dgcr5 silence on propofol caused huh‐7 and hep g2 cell viability loss, proliferation inhibition, migration and invasion suppression, apoptosis induction, as well as raf1/erk1/2 and wnt/β‐catenin pathways inactivation were assessed, respectively.We discovered that propofol declined huh‐7 and hep g2 cell viability, proliferation, migration and invasion, but increased cell apoptosis.Dgcr5 had a relatively lower expression level in hepatocellular carcinoma tissues and cells.Propofol elevated dgcr5 expression in huh‐7 and hep g2 cells.Increased expression of dgcr5 was connected with the anticancer activity of propofol on huh‐7 and hep g2 cells.Besides, propofol repressed raf1/erk1/2 and wnt/β‐catenin pathways through elevating dgcr5 expression.In conclusion, the anticancer activity of propofol on hepatocellular carcinoma was verified in this study.Propofol repressed hepatocellular carcinoma huh‐7 and hep g2 cell growth and metastasis at least by elevating dgcr5 and hereafter inactivating raf1/erk1/2 and wnt/β‐catenin pathways.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
CBP-triggered KDM2B acetylation accelerates the carcinogenesis of colon cancer

Lysine (k)‐specific demethylase 2b (kdm2b) has been testified to be an oncogene in diverse cancers, which joins in mediating the carcinogenesis of cancers.Nonetheless, the function of kdm2b in colon cancer remains unexplored.The study attempted to disclose the influences of kdm2b acetylation in the progression of colon cancer.Sw48 and sun‐c1 cells were transfected with flag‐kdm2b and administrated by trichostatin a and nicotinamide for 24 hr.Immunoprecipitation with a flag antibody followed by western blot with acetyl‐lysine‐specific antibody was executed to detect kdm2b acetylation.The correlation between creb binding protein (cbp) and kdm2b was then investigated.The k‐r and k‐q mutants were constructed and the impacts of kdm2b on demethylation of nucleosomal substrates, p21, and puma transcription and the carcinogenesis of colon cancer were probed.Cbp immediately evoked kdm2b acetylation at lysine residue 765 in colon cancer cells.Acetylation of kdm2b obviously destroyed the relevance with nucleosomes, demethylation of nucleosomal substrates, and repressed p21 and puma transcription.More important, kdm2b acetylation restrained sun‐c1 cells proliferation and colony formation, meanwhile, hindered cell migration and invasion.Beyond that, the tumor formation was repressed by kdm2b acetylation.The observations testified that cbp‐triggered kdm2b acetylation accelerated the carcinogenesis of colon cancer.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
EZH2 regulates H2B phosphorylation and elevates colon cancer cell autophagy

Epigenetic alterations, especially histone modification, play vital roles in the pathogenesis of colon cancer.Upregulation of the enhancer of zeste homolog 2 (ezh2) has been reported to contribute to the initiation and progression of colon cancer.This study analyzed the association between ezh2 and phosphorylation of h2b at tyrosine 37 (h2b y37ph ) in colon cancer tissues and cells, along with the influences of the ezh2‐h2b y37ph axis on colon cancer cell autophagy.Immunohistochemistry was utilized to assess ezh2 and h2b y37ph expressions in clinical samples of colon cancer.Cell transfection was carried out to alter ezh2 and h2b y37ph expressions in colon cancer cells.Co‐immunoprecipitation analysis and glutathione‐s‐transferase (gst) pull down assay were conducted to analyze the association between ezh2 and h2b y37ph .Western blotting was utilized to measure proteins expressions related to cell autophagy.We found that there was a positive association between ezh2 and h2b y37ph in colon cancer tissues and cells.Ezh2 directly interacted with h2b and promoted h2b y37ph in colon cancer cells using atp as a phosphate donor.Moreover, ezh2 levated colon cancer cell autophagy in starvation condition.H2b y37ph was required for ezh2‐elevated colon cancer cell autophagy under starvation condition.The ezh2‐h2b y37ph axis elevated colon cancer cell autophagy possibly via activating transcriptional regulation of atg genes.In conclusion, ezh2‐elevated colon cancer initiation and progression at least in part via inducing colon cancer cell autophagy.Ezh2 could phosphorylate h2b y37 and then induce transcription activation of atg genes in colon cancer cells under starvation condition.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
MicroRNA-204-3p represses colon cancer cells proliferation, migration, and invasion by targeting HMGA2

Colon cancer is a detrimental neoplasm of the digestive tract.Micro rnas (mi rnas) as central regulators have been discovered in colon cancer.Nonetheless, the impact of mi r‐204‐3p on colon cancer remains indistinct.The research attempted to uncover the impacts of mi r‐204‐3p on colon cancer cells growth, migration, and invasion.Mi r‐204‐3p expression level in colon cancer tissues and diverse colon cancer cell lines were testified by the quantitative real‐time polymerase chain reaction.Exploration of the impacts of mi r‐204‐3p on cell growth, migration, invasion, and their associated factors through assessment of cck‐8, flow cytometry, transwell, and western blot, respectively.High mobility group at‐hook 2 (hmga2) expression was then detected in caco‐2 cells after mi r‐204‐3p mimic and inhibitor transfection, additionally dual‐luciferase activity was implemented to further uncover the correlation between hmga2 and mi r‐204‐3p.The impact of hmga2 on caco‐2 cell growth, migration, and invasion was finally assessed.We found that repression of mi r‐204‐3p was discovered in colon cancer tissues and hct116, sw480, caco‐2, ht29 and sw620 cell lines.Mi r‐204‐3p overexpression mitigated coca‐2 cell viability, facilitated apoptosis, simultaneously adjusted cyclin d1 and cleaved caspase‐3 expression.Cell migration, invasion, and the associated factors were all suppressed by mi r‐204‐3p overexpression.Reduction of hmga2 was presented in caco‐2 cells with mi r‐204‐3p mimic transfection, and hmga2 was predicated to be a target gene of mi r‐204‐3p.Besides, hmga2 silence showed the inhibitory effect on caco‐2 cells growth, migration, and invasion.In conclusion, mi r‐204‐3p repressed colon cancer cell growth, migration, and invasion through targeting hmga2.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
MicroRNA-132 protects H9c2 cells against oxygen and glucose deprivation-evoked injury by targeting FOXO3A

Myocardial ischemia/reperfusion injury (miri) is a clinically familiar disease, which possesses a great negative impact on human health.But, the effective treatment is still absent.Micro rnas (mi rnas) have been testified to play a momentous role in miri.The purpose of the study aimed to probe the functions of mi r‐132 in oxygen and glucose deprivation (ogd)‐evoked injury in h9c2 cells.Mi r‐132 expression in h9c2 cells accompanied by ogd disposition was evaluated via real‐time quantitative polymerase chain reaction.After mi r‐132 mimic and inhibitor transfections, the impacts of mi r‐132 on ogd‐affected h9c2 cell viability, apoptosis, cell cycle, and the interrelated factors were appraised by exploiting cell counting kit‐8, flow cytometry, and western blot analysis.Foxo3a expression was estimated in above‐transfected cells, meanwhile, the correlation between mi r‐132 and foxo3a was probed by dual‐luciferase report assay.Ultimately, above mentioned cell processes were reassessed in h9c2 cells after preprocessing ogd administration and transfection with si‐foxo3a and si‐nc plasmids.We got that ogd disposition obviously enhanced mi r‐132 expression in h9c2 cells.Overexpressed mi r‐132 evidently reversed ogd‐evoked cell viability repression and apoptosis induction in h9c2 cells.In addition, overexpressed mi r‐132 mitigated ogd‐evoked g0/g1 cell arrest by mediating p21, p27, and cyclin d1 expression.Repression of foxo3a was observed in mi r‐132 mimic‐transfected cells, which was also predicated as a direct gene of mi r‐132.We discovered that silenced foxo3a alleviated ogd‐evoked cell injury in h9c2 cells via facilitating cell viability, hindering apoptosis and restraining cell arrest at g0/g1 phase.In conclusion, these investigations corroborated that mi r‐132 exhibited the protective impacts on h9c2 cells against ogd‐evoked injury via targeting foxo3a.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
LncRNA-ROR alleviates hypoxia-triggered damages by downregulating miR-145 in rat cardiomyocytes H9c2 cells

Chronic hypoxic heart disease (chd) is a common clinical type of congenital heart disease.Long noncoding rna regulator of reprogramming (lnc rna‐ror) exerts an important regulating effect in cardiovascular diseases.In our study, we explored the effect of lnc rna‐ror and the possible mechanisms against hypoxia‐caused apoptosis in h9c2 cells.H9c2 cells were exposed to hypoxia (1% o 2 ) to construct the in vitro model of chd.The level of lnc rna‐ror and micro rna (mi rna/mi r)‐145 was detected.To upregulate the level of lnc rna‐ror and mi r‐145, transfection was carried out.Western blot assay was performed to quantified protein expression.The interaction of lnc rna‐ror with mi r‐145 was verified by rip and dual‐luciferase reporter assays.The expression of p53 and bax was largely elevated and bcl‐2 was suppressed by hypoxia induction.We found that lnc rna‐ror was elevated by hypoxia.Lnc rna‐ror overexpression was able to relieve the damages of h9c2 cells induced by hypoxia through rescuing viability, suppressing apoptosis, and blocking cytochrome c release.Mi r‐145 was suppressed by overexpressed lnc rna‐ror and the combination of mi r‐145 mimic was able to abolish the protective effect of lnc rna‐ror.Moreover, we found that lnc rna‐ror activated ras/raf/mek/erk and pi3k/akt transduction cascades by suppressing mi r‐145.Besides, lnc rna‐ror directly targeted mi r‐145 and negatively modulated the level of mi r‐145.Our present study revealed that lnc rna‐ror protected h9c2 cells against hypoxia‐caused damages by regulation of mi r‐145 through activating ras/raf/mek/erk and pi3k/akt.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
Long noncoding RNA MEG3 is a tumor suppressor in choriocarcinoma by upregulation of microRNA-211

Tumor suppressor long noncoding rna maternally expressed gene 3 (lnc rna meg3) exists in various cancers.Nonetheless, the functions of lnc rna meg3 in choriocarcinoma (cc) are still not well studied.We explored the effects of lnc rna meg3 on human cc jeg‐3 and be wo cells.Lnc rna meg3 was overexpressed, and the effects of lnc rna meg3 on cell viability, proliferation, apoptosis, migration, and invasion were assessed by the cell counting kit‐8 assay, western blot analysis, flow cytometry (plus western blot analysis), and transwell assay (plus western blot analysis), respectively.Then, the expression level of mi r‐211 was detected by real‐time quantitative polymerase chain reaction.After that, the effects of dysregulated micro rna‐211 (mi r‐211) with overexpressing lnc rna meg3 on jeg‐3 cells and be wo cells were testified.Western blot analysis was used to study the involvements of the signaling pathways in the lnc rna meg3‐associated modulation.We found that lnc rna meg3 upregulation reduced cell viability, inhibited proliferation, migration and invasion, and promoted apoptosis.Expression of mi r‐211 was upregulated after lnc rna meg3 overexpression.Effects of lnc rna meg3 overexpression were augmented by mi r‐211 overexpression, while they were declined by mi r‐211 silencing.Phosphorylated levels of pi3k, akt, and amp‐activated protein kinase (ampk) were decreased by lnc rna meg3 overexpression via regulation of mi r‐211.To sum up, lnc rna meg3 could repress proliferation, migration and invasion, and promote apoptosis of jeg‐3 and be wo cells through upregulating mi r‐211.The pi3k/akt and ampk pathways were inhibited by lnc rna meg3 overexpression via regulation of mi r‐211.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;