syedzayyan/paper_mill_benchmark huggingface dataset:
MiR-16-5p inhibits breast cancer by reducing AKT3 to restrain NF-kB pathway

Background: breast cancer endangers the life of women and has become the major cause of deaths among them.Mi rnas are found to exert a regulatory effect on the migration, proliferation and apoptosis of breast cancer cells.This research aims at investigating the mi r-16-5p expression and its effect on the pathogenesis of breast cancer.Methods: their clinical data were analyzed with q rt-pcr.Cck8, ed u and transwell was performed to explore the function of mi r-16-5p in cell migration and proliferation of breast cancer cells.Dual-luciferase reporter assay, immunohistochemistry and western blotting were carried out to explore the relation between mi r-16-5p and akt3.Results: it was discovered that mi r-16-5p was lowly expressed in breast cancer patients.Meanwhile, breast cancer patients with under-expressed mi r-16-5p had a lower survival rate than those with highly expressed mi r-16-5p.Furthermore, decreased mi r-16-5p in cell and animal models enhanced migration and proliferation of breast cancer cells, stimulated cell cycle and reduced cell apoptosis.Finally, we found mi r-16-5p restrained the nf-κb pathway and decreased akt3 gene, thereby suppressing the breast cancer development.Conclusion: it can be seen that mi r-16-5p exhibits a low expression in breast cancer tissues, which can inhibit breast cancer by restraining the nf-κb pathway and elevating reducing akt3.

Journal: Bioscience Reports (2019)
Publication types: Research Article;
Down-Regulation of MiR-150 Alleviates Inflammatory Injury Induced by Interleukin 1 via Targeting Kruppel-Like Factor 2 in Human Chondrogenic Cells

Interleukin-1 (il-1) is known to be involved in cartilage degeneration following joint injury or due to osteoarthritis.In the present study, we explored the effects of mi r-150 on il-1-stimulated human chondrogenic cells atdc5.Methods: atdc5 cells were transfected with the mimic, inhibitor or negative controls specific for mi r-150, and subsequently treated by il-1.Cck8 assay, pi and fitc-conjugated annexin v double-staining, western blot, q rt-pcr and elisa assay were performed to determine the changes of cell viability, apoptosis, and the release of pro-inflammatory cytokines.Targeting relationship between mi r-150 and klf2 was detected by dual luciferase activity assay.Results: il-1 reduced cell viability, induced apoptosis, and enhanced the expression and release of pro-inflammatory cytokines (il-6, il-8 and tnf-α) in atdc5 cells.Il-1 also increased the expression of mi r-150.Suppression of mi r-150 alleviated il-1-induced cell damage in atdc5 cells, while overexpression of mi r-150 resulted in an opposite impact.Klf2 was negatively regulated by mi r-150, and it was proved as a target gene of mi r-150.Klf2 overexpression exhibited protective actions in il-1-injured atdc5 cells, even if mi r-150 was suppressed in cell.Moreover, il-1-induced activation of nf-k b and notch pathways was alleviated by klf2 overexpression.Conclusions: suppression of mi r-150 led to up-regulation of klf2, which in turn protected atdc5 cells against il-1-induced injury.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Lycium Barbarum Polysaccharides Alleviates Oxidative Damage Induced by H2O2 Through Down-Regulating MicroRNA-194 in PC-12 and SH-SY5Y Cells

Currently, scientists attempt to improve outcome of spinal cord injury (sci) via reducing secondary injury during sci.Oxidative stress is critical for pathophysiology of secondary damage, thus we mainly focused on the anti-oxidant effects of lycium barbarum polysaccharides (lbps) on pc-12 and sh-sy5y cells as well as the underlying mechanisms.Methods: oxidative stress was induced by h2o2 stimulation.Effects of lbps on cell viability, apoptosis, and expression of proteins associated with apoptosis and autophagy in h2o2-induced cells were assessed by cck-8 assay, flow cytometry assay and western blot analysis, respectively.Then, expression of mi r-194 was determined by q rt-pcr.Expression of mi r-194 was dysregulated, and whether lbps affected h2o2-treated cells through modulating mi r-194 was verified.The expression of key kinases in the pi3k/akt pathway and the intracellular levels of ros and no were testified by western blot analysis and flow cytometry with fluorescent probes.Results: h2o2-induced decrease of cell viability and increases of apoptosis and autophagy in pc-12 cells were mitigated by lbps treatment.Next, we found that mi r-194 expression was both down-regulated by lbps treatment in pc-12 and sh-sy5y cells.More experiments consolidated that influence of lbps on h2o2-treated cells was reversed by mi r-194 overexpression while was augmented by mi r-194 inhibition.Lbps elevated the phosphorylated levels of pi3k and akt and reduced levels of ros and no through mi r-194.Conclusion: lbps alleviated h2o2-induced decrease of cell viability, and increase of apoptosis and autophagy through down-regulating mi r-194.Moreover, lbps activated the pi3k/akt pathway and reduced oxidative stress through mi r-194.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Schizandrin A Alleviates LPS-Induced Injury in Human Keratinocyte Cell Hacat Through a MicroRNA-127-Dependent Regulation

Inflammatory skin diseases are the most common problems in dermatology.Schizandrin a (sch a) has been reported to have anti-inflammatory properties.Herein, we aimed to investigate the protective effects of sch a on lipopolysaccharide (lps)-induced injury in keratinocyte ha ca t cells.Methods: inflammation injury in ha ca t cells was induced by lps treatment.Cell viability, apoptotic cell rate, and apoptosis-related proteins were analyzed by cell counting kit-8 (cck-8) assay, annexin v-(fluorescein isothiocyanate (fitc)/ propidium iodide (pi) double staining method, and western blot, respectively.The pro-inflammatory factors were analyzed by western blot and quantified by enzyme linked immunosorbent assay (elisa).Expression of mi r-127 in sch a-treated cells was analyzed by q rt-pcr.The effects of sch a on activations of p38mapk/erk and jnk pathways were analyzed by western blot.Results: sch a protected ha ca t cells from lps-induced inflammation damage via promoting cell viability, suppressing apoptosis.Meanwhile, sch a inhibited il-1β, il-6, and tnf-α expression.Mi r-127 expression was up-regulated in lps-treated ha ca t cells but down-regulated after sch a treatment.Overexpression of mi r-127 inhibited cell growth and induced expression of il-1β, il-6 and tnf-α.Additionally, mi r-127 overexpression impaired the protective effects of sch a, implying mi r-127 might be correlated to the anti-inflammation property of sch a and also involved in inactivation of p38mapk/erk and jnk pathways by sch a.Conclusion: mi r-127 is involved in the protective functions of sch a on lps-induced inflammation injury in human keratinocyte cell ha ca t, which might inactivates of p38mapk/erk and jnk signaling pathways in ha ca t cells.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

Melanoma is one of the most aggressive malignant tumors, with increasing incidence, poor prognosis, and lack of any effective targeted therapies.Abnormal expression of mi r-29a has been found in several types of cancers, including melanoma.In this study, experiments were performed to investigate the role of mi r-29a in melanoma, and the molecular mechanism by which mi r-29a represses melanoma.Methods: mi r-29 and bmi1 expression was examined by quantitative real-time polymerase chain reaction (q rt-pcr).The cell viability, apoptosis, migration and invasion were respectively determined by cell counting kit-8 assay, propidium iodide (pi) fluorescein isothiocynate (fitc)-annexin v staining assay, wound healing assay and transwell assay.Luciferase reporter assay was performed to determine a target gene of mi r-29a.Western blot was used to analyze protein expression of apoptosis-related proteins, bmi1, wnt/β-catenin and nuclear factor-κb (nf-κb) pathway target genes.Results: mi r-29a was down-regulated in all tested melanoma cell lines.Up-regulation of mi r-29a effectively inhibited cell viability, migration, and invasion, but promoted apoptosis in a375 cells.Bmi1 was a direct target gene of mi r-29a.Transfection with mi r-29a mimic decreased cell migration and invasion and bmi1 expression in malme-3m cells, sk-mel-2, sk-mel-5, and m14 cell lines.Moreover, mi r-29a might suppress growth, migration and invasion of a375 cells by negatively regulating bmi1.In addition, our results demonstrated that transfection with mi r-29a mimic effectively blocked wnt/β-catenin and nf-κb pathways via down-regulating bmi1.Conclusion: mi r-29a could be functioned as a potential tumor suppressor through direct regulation of bmi1 in melanoma cells.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Resveratrol (rsv) has been reported as a promising oral supplementation for osteoarthritis treatment, while the mechanism of its action is still unclear.The specific aim of this study is to decode one of the mechanisms by which rsv protects chondrocyte.Methods: mouse chondrogenic cell line atdc5 was treated with 30 μm rsv for 24 h, and 10 μg/ml lps for 12 h, after which cell viability, apoptosis, and the release of pro-inflammatory cytokines were assessed.The expression of mi r-146b in atdc5 cells was silenced by the specific inhibitor transfection, and then cell viability, apoptosis and inflammation were re-assessed.Results: the ic50 value of lps in atdc5 cells was about 10.27 μg/ml.Lps with a dosage of 10 μg/ml repressed cell viability, induced apoptosis, and increased the release of il-1β, il-6 and tnf-α.Rsv pre-treatment (30 μm) significantly alleviated lps-induced apoptosis and inflammation.More importantly, mi r-146b was up-regulated by rsv, and the protective functions of rsv on atdc5 cells were attenuated by mi r-146b silence.Further, nf-κb and p38mapk pathways were activated by lps, and were deactivated by rsv.Besides, rsv-induced the deactivation of nf-κb and p38mapk pathways was reversed by mi r-146b silence.Conclusions: our findings suggest that rsv protects atdc5 cells from lps-induced inflammatory and apoptotic injury via up-regulation of mi r-146b and thereby deactivation of nf-κb and p38mapk pathways.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Ligustrazine Inhibits Growth, Migration and Invasion of Medulloblastoma Daoy Cells by Up-Regulation of miR-211

Ligustrazine (lsz) has been identified as an antitumor agent against some types of cancers.Nevertheless, its ability to inhibit growth, migration and invasion of medulloblastoma cells is still unclear.This study aimed to explore the effect of lsz on daoy cells.Methods: the effects of lsz on viability, proliferation, apoptosis, migration, and invasion of daoy cells were analyzed by cck-8, brd u, flow cytometry and transwell assays, respectively.The effect of lsz on mi r-211 expression was analyzed by q rt-pcr.Mi r-211 inhibitor transfection was performed to suppress mi r-211 expression.The effects of lsz on apoptosis-related factors, mmp-2, mmp-9, and vimentin (vim), as well as main factors of pi3k/akt and m tor pathways were analyzed by western blot.Results: lsz inhibited viability but promoted apoptosis of daoy cells.Additionally, the proliferative, migratory and invasive abilities of daoy cells were decreased by lsz.Meanwhile, lsz promoted the activations of caspase-3 and caspase-9, increased bax level, decreased bcl-2 level, as well as inhibited the expressions of mmp-2, mmp-9 and vim.Additionally, we found that lsz enhanced mi r-211 expression and exerted its anti-medulloblastoma effect by up-regulation of mi r-211.Furthermore, lsz inhibited pi3k/akt and m tor signaling pathways by up-regulating mi r-211.Conclusion: lsz suppressed medulloblastoma daoy cells by up-regulating mi r-211 and further modulating the activations of pi3k/akt and m tor signaling pathways.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Recent studies have suggested that several lnc rnas contribute to the angiogenic function of endothelial cells.Herein, we set out to reveal whether lnc rna uca1 has functions in endothelial angiogenesis.Methods: the expression levels of lnc rna uca1, mi r-195 and ccnd1 in human microvascular endothelial hmec-1 cells were altered by transfection.Subsequently, cell viability, migration, tube formation and apoptosis of hmec-1 cells were respectively assessed.The cross-talk between lnc rna uca1, mi r-195, ccnd1, and mek/erk and m tor signaling pathways were investigated by performing q rt-pcr and western blotting.Results: silence of lnc rna uca1 repressed hmec-1 cells viability, migration, tube formation, and induced apoptosis.Meanwhile, silence of lnc rna uca1 significantly up-regulated mi r-195 expression.These alterations induced by lnc rna uca1 were further enhanced by mi r-195 overexpression, while were attenuated by mi r-195 suppression.Moreover, silence of lnc rna uca1 deactivated mek/erk and m tor signaling pathways via a mi r-195-dependent regulation.And the deactivation of mek/erk and m tor signaling pathways led to a down-regulation of ccnd1.Conclusion: this study demonstrates that silence of lnc rna uca1 largely represses microvascular endothelial cells growth and tube formation.Silence of lnc rna uca1 exerts its function possibly via up-regulation of mi r-195, which in turn inactivates mek/erk and m tor signaling pathways, and ultimately represses ccnd1 expression.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MiR-1246 Promotes LPS-Induced Inflammatory Injury in Chondrogenic Cells ATDC5 by Targeting HNF4γ

Osteoarthritis (oa) is a common inflammatory joint disease.Mi rnas are associated with oa and functionally implicated in the pathogenesis of the disease.In the present study, we investigated the role of mi r-1246 in the lipopolysaccharide (lps)-induced inflammatory injury of atdc5 cells.Methods: atdc5 cells were cultured and treated with lps in a series of concentration (0, 1, 5, and 10 μg/ml) for 5 h.The cells were transfected with mi r-1246-mimic, inhibitor, si-hnf4γ or negative control, then were assessed for cell viability using cck8 assay, apoptosis by flow-cytometry and expressions of mi r-1246 and pro-inflammatory cytokines by q rt-pcr and western blot analysis.Results: cell viability was significantly reduced and cell apoptosis was added in atdc5 cells injured with lps at the dosage of 5 and 10 μg/ml.Relative m rna expressions of pro-inflammatory cytokines (il-1β, il-6, il-8 and tnf-α) were significantly increased.Mi r-1246 was up-regulated in atdc5 cells treated with lps.Moreover, mi r-1246 overexpression aggravated lps-induced decrease in cell viability, increase in apoptosis and overproduction of pro-inflammatory factors.M rna and protein expressions of hnf4γ were significantly suppressed in cells transfected with mi r-124-mimic.Further, mi r-1246 knockdown alleviated lps-induced inflammatory injury by up-regulating the expression of hnf4γ and activation of pi3k/akt and jak/stat pathways.Conclusions: suppression of mi r-1246 alleviated lps-induced inflammatory injury in chondrogenic adtc5 cells by up-regulation of hnf4γ and activation of pi3k/akt and jak/stat pathways.The findings of this study will provide a novel viewpoint regarding mi r-1246 target for clinical.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
Ganoderic Acid A Protects Rat H9c2 Cardiomyocytes from Hypoxia-Induced Injury via Up-Regulating miR-182-5p

Ganoderic acid a (gaa) isolated from ganoderma lucidum, shows various benefit activities, such as anti-tumor activity, anti-hiv activity and hepatoprotective activity.However, the potential effects of gaa on hypoxia-induced injury of cardiomyocytes are still unclear.In this study, we aimed to reveal the effects of gaa on hypoxic-induced h9c2 cell injury, as well as potential underlying molecular mechanisms.Methods: rat h9c2 cardiomyocytes were cultured in hypoxia condition with different doses of gaa.Cell viability and apoptosis were detected by cck-8 assay and flow cytometry, respectively.Q rt-pcr was performed to assess the expression levels of micro rna-182-5p (mi r-182-5p) and phosphatase and tensin homologue (pten).Cell transfection was conducted to change the expression levels of mi r-182-5p and pten in h9c2 cells.Finally, protein levels of key factors involved in cell proliferation, cell apoptosis and pten/pi3k/akt pathway were evaluated using western blotting.Results: hypoxia treatment significantly induced h9c2 cell viability loss and apoptosis.Gaa incubation remarkably protected h9c2 cells from hypoxia-induced viability loss, proliferation inhibition and apoptosis.In addition, gaa obviously enhanced the expression level of mi r-182-5p in h9c2 cells.Suppression of mi r-182-5p notably alleviated the protective effects of gaa on hypoxia-treated h9c2 cells.Furthermore, mi r-182-5p negatively regulated the m rna and protein levels of pten in h9c2 cells.Gaa attenuated hypoxia-induced inactivation of pi3k/akt pathway in h9c2 cells by up-regulating mi r-182-5p and then down-regulating pten.Conclusion: gaa protected rat h9c2 cardiomyocytes from hypoxia-induced injury might via up-regulating mi r-182-5p, down-regulating pten and then activating pi3k/akt signaling pathway.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MicroRNA-486 Alleviates Hypoxia-Induced Damage in H9c2 Cells by Targeting NDRG2 to Inactivate JNK/C-Jun and NF-κB Signaling Pathways

Acute myocardial infarction is a serious disease with high morbidity and mortality.Micro rnas (mi rnas) have been proved to play an important role in modulating myocardial ischemia and reperfusion injury.Hence, in this study, we constructed h9c2 cell model to elucidate the roles of micro rna-486 (mi r-486) in preventing hypoxia-induced damage in h9c2 cells.Methods: h9c2 cells were cultured in hypoxic incubator with 1% o2 to simulate hypoxia and/or transfected with mi r-486 mimic, scramble, anti-mi r-486, si-n-myc downstream-regulated gene 2 (ndrg2) and their corresponding negative controls (nc).Effects of mi r-486 and/or ndrg2 dysregulation on hypoxia-induced myocardial injury in h9c2 cells were investigated by evaluating cell viability, migration, invasion and apoptosis using cell counting kit-8 (cck-8), transwell assay, flow cytometry, respectively.The proteins expression and rna expression were detected by western blot and quantitative real time polymerase chain reaction (q rt-pcr), respectively.Results: hypoxia treatment induced damage in h9c2 cells by decreasing cell viability, migration and invasion and increasing cell apoptosis.Moreover, hypoxia inhibited the expression of mi r-486 in h9c2 cells.Overexpression of mi r-486 alleviated hypoxia-induced myocardial injury in h9c2 cells, while suppression of mi r-486 further aggravated hypoxia-induced injury.Furthermore, ndrg2 expression was negatively regulated by mi r-486, and ndrg2 was confirmed as a target of mi r-486.Knockdown of ndrg2 alleviated the effects of mi r-486 suppression on hypoxia-induced myocardial injury.Besides, knockdown of ndrg2 markedly inhibited the activation of c-jun n-terminal kinase (jnk) /c-jun and nuclear factor κb (nf-κb) signaling pathways in hypoxia-induced h9c2 cells.Conclusion: our findings indicate that mi r-486 may alleviate hypoxia-induced myocardial injury possibly by targeting ndrg2 to inactivate jnk/c-jun and nf-κb signaling pathways.Mi r-486 may be a potential target for treating ischemic myocardial injury following acute myocardial infarction.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Chinese medicine Di-Huang-Yi-Zhi protects PC12 cells from H2O2-induced apoptosis by regulating ROS-ASK1-JNK/p38 MAPK signaling

Background oxidative stress mediates the nerve injury during the pathogenesis of alzheimer’s disease (ad).Protecting against oxidative stress damage is an important strategy to prevent and treat ad.Di-huang-yi-zhi (dhyz) is a chinese medicine used for the treatment of ad, but its mechanism remains unknown.This study is aimed to investigate the effect of dhyz on h 2 o 2 induced oxidative damage in pc12 cells.Methods pc12 cells were treated with h 2 o 2 and dhyz.Cell proliferation was detected by cell counting kit-8 (cck-8) assay.Cytotoxicity of h 2 o 2 was measured by lactate dehydrogenase (ldh) release assay.Apoptosis were identified by annexin v-fitc/pi staining.Caspase 3 activity was detected by commercial kit.Mitochondrial membrane potential (mmp) was detected by jc-1 staining.Reactive oxygen species (ros) was 2′, 7′-dichlorodihydrofluorescein diacetate (dcfh-da) staining.Protein expression and phosphorylation was identified by western blot.Results the results showed that dhyz antagonized h 2 o 2 -mediated cytotoxicity and proliferation inhibition.Dhyz reduced ros production, stabilize mitochondrial membrane potential, inhibit caspase-3 activity and apoptosis induced by h 2 o 2 .In addition, dhyz inhibited the phosphorylation of ask1, jnk1/2/3 and p38 mapk which were up-regulated by h 2 o 2 .Conclusions the present study suggested that dhyz protected pc12 cells from h 2 o 2 -induced oxidative stress damage and was related to inhibition of ros production and ask1-jnk/p38 mapk signaling.The present study provides experimental evidence for the application of dhyz for the management of oxidative stress damage and ad.

Journal: BMC Complementary Medicine and Therapies (2020)
Publication types: Research Article;
MicroRNA-96-5p promotes proliferation, invasion and EMT of oral carcinoma cells by directly targeting FOXF2

Recently, micro rna-96-5p (mi r-96-5p) has been reported to function as both a tumor suppressor and oncogene in several cancer types, including gastric cancer, hepatocellular cancer and lung cancer.However, the biological function of mi r-96-5p and its precise mechanisms in oral squamous cell carcinoma (oscc) have not been well clarified.The aim of this study was to study the roles of mi r-96-5p/foxf2 axis in oscc.In this study, the mi r-96-5p level was dramatically enhanced in oscc tissues and cell lines, and the foxf2 expression was significantly reduced.In addition, the foxf2 expression was negatively related to the mi r-96-5p level in oscc tissues.Furthermore, downregulation of mi r-96-5p obviously restrained oscc cell proliferation, invasion and emt.We confirmed that mi r-96-5p could directly target foxf2 by luciferase reporter assay.Moreover, knockdown of foxf2 also could markedly promote the proliferation, invasion and emt of oscc cells.Finally, overexpression of foxf2 in oscc cells partially reversed the promoted effects of mi r-96-5p mimic.Knockdown of mi r-96-5p restrained oscc cells proliferation, invasion and emt via regulation of foxf2.

Journal: Biology Open (2020)
Publication types: Research Article;