syedzayyan/paper_mill_benchmark huggingface dataset:
Ligustrazine protects chondrocyte against IL-1β induced injury by regulation of SOX9/NF-κB signaling pathway

Ligustrazine is extracted from rhizoma ligustici wallichii , is known for its vasodilatory properties in the traditional chinese herbal medicine.The study aimed to determine the effect and the underlying mechanism of ligustrazine on interleukin‐1β (il‐1β)‐induced injury in osteoarthritis (oa).Human articular cartilages and joint effusion were obtained from patients with oa, and the chondrocytes were isolated and treated with il‐1β.The different inflammatory cytokines were analyzed by elisa.Cell viability, apoptosis, and apoptosis‐related factors were examined by mtt, flow cytometry, and western blot.Then, the expressions of col2a1 and acan , and the concentrations of s gag and mmp‐13 were measured.The level of sod and mda and ros production were then analyzed.Furthermore, the protein levels of sox9 and nf‐κb pathway were detected by western blot.Ligustrazine significantly suppressed inflammatory reaction in joint effusion of oa patients.Moreover, ligustrazine attenuated il‐1β‐induced chondrocytes injury and matrx degradation in chondrocytes.Ligustrazine promoted oxidative stress response by increasing sod level, decreasing mda level, and inhibiting ros production in il‐1β‐induced chondrocytes.Besides, ligustrazine increased sox9 expression, and sox9 silencing reversed the effect of ligustrazine on matrx degradation in il‐1β‐injured chondrocytes.Furthermore, ligustrazine blocked nf‐κb pathway in il‐1β‐induced chondrocytes, and ptdc (nf‐κb inhibitor) enhanced the effect of ligustrazine on viability, apoptosis, sox9 expression, and ros production in il‐1β‐induced chondrocytes.These results indicated that ligustrazine protected chondrocytes against il‐1β‐induced injury possibly by regulation of sox9 and inactivation of nf‐κb signaling pathway.It could act as a therapeutic agent for the treatment of oa.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Long non-coding RNA GAS5 aggravates hypoxia injury in PC-12 cells via down-regulating miR-124

One important feature of cerebral ischemia is hypoxia injury in nerve cells.Growth arrest‐specific transcript 5 (gas5) is widely reported as a tumor suppressor gene; however, the investigations about its role in cerebrovascular disease are relatively rare.This study was aimed to explore the impact of gas5 on hypoxia response in nervous cells.Pc‐12 cells were incubated under anoxic condition to induce hypoxia injury.Regulatory effects of gas5 on mi r‐124 and mi r‐124 on icam‐1 expression were assessed by q rt‐pcr and/or western blot.Targeting effect of mi r‐124 on icam‐1 3′‐untranslated regions (utr) was evaluated through dual luciferase activity assay.The potential regulatory mechanism on hypoxia injury in pc‐12 cells was assessed by detecting key elements of nf‐κb and notch signaling pathways using western blot.Gas5 ectopic expression accentuated hypoxia injury in pc‐12 cells.Mi r‐124 expression was negatively regulated by gas5 expression.Cells with overexpressions of gas5 and mi r‐124 alleviated hypoxia injury as in compassion with cells only with gas5 overexpression.Icam‐1 expression was negatively regulated by mi r‐124 expression.Icam‐1 was a functional target of mi r‐124.Icam‐1 overexpression aggravated hypoxia injury, but inversely, icam‐1 silence diminished hypoxia damage.Besides, icam‐1 expression was negatively related with activation of nf‐κb and notch pathways.Gas5‐mi r‐124‐icam‐1 axis could regulate hypoxia injury in pc‐12 cells.Gas5 might aggravate hypoxia injury via down‐regulating mi r‐124, then up‐regulating icam‐1, and further enhancing activations of nf‐κb and notch pathways.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-132 attenuates LPS-induced inflammatory injury by targeting TRAF6 in neuronal cell line HT-22

Epilepsy is a common neurological disorder in the central nervous system.Inflammation disrupts the blood‐brain barrier (bbb), which is responsible for maintaining brain homeostasis.This study was aimed to investigate the functional role of micro rna (mi r)‐132 in hippocampal ht‐22 cells under lipopolysaccharide (lps) stimulation.In vitro cell inflammatory model was constructed by lps stimulation.Inflammatory cell injury was evaluated according to the alterations of cell viability, apoptosis, and expression of inflammatory cytokines.Then, mi r‐132 level after lps treatment was assessed.Subsequently, mi r‐132 was abnormally expressed after cell transfection, and the effects of mi r‐132 on lps‐induced cell inflammatory injury as well as phosphorylated levels of key kinases in the nf‐κb and mapk kinase (mek)/erk pathways were determined.The target gene of mi r‐132 was virtually screened and verified, and whether mi r‐132 affected ht‐22 cells under lps stimulation through regulating the target gene was verified.The results showed that the level of mi r‐132 was down‐regulated by lps in ht‐22 cells, and the lps‐induced inflammatory injury could be reduced by mi r‐132 overexpression.Then, the phosphorylated levels of kinases in the nf‐κb and mek/erk pathways were decreased by mi r‐132 overexpression.Tumor necrosis factor receptor‐associated factor 6 (traf6) was predicted and verified to be a target of mi r‐132.Moreover, the alterations induced by mi r‐132 overexpression in the lps‐treated ht‐22 cells were abrogated by traf6 overexpression.Therefore, we drew the conclusion that lps down‐regulated mi r‐132 and mi r‐132 attenuated lps‐induced inflammatory cell injury by targeting traf6, along with the inhibition of the nf‐κb and mek/erk pathways.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Ginsenoside Rh2 inhibits proliferation and migration of medulloblastoma Daoy by down-regulation of microRNA-31

This study aimed to investigate the effects of ginsenoside rh2 on proliferation, apoptosis, and migration of the human medulloblastoma cell line daoy, as well as to explore the potential mechanisms of the effects.The human medulloblastoma cell line daoy was cultured in vitro and treated with or without ginsenoside rh2.Cck‐8 assay was performed to investigate the effect of rh2 on cell survival using a cell counting kit‐8.Cell proliferation was assessed by brd u assay.Cell apoptosis was determined using flow cytometry analysis.Cell migration was detected using a modified two‐chamber migration assay.Mi r‐31 mimic and the nc control were transfected into daoy cells and detected by q rt‐pcr.The expression of wnt3a, wnt5a, and β‐catein was detected by western blot analysis.Rh2 efficiently suppressed the proliferation and migration, and promoted the apoptosis of daoy cells.Additionally, rh2 could down‐regulate mi r‐31.Mi r‐31 overexpression reversed the effects of rh2 on proliferation, apoptosis and migration of daoy cells, and activated the wnt/β‐catein signaling pathways in daoy cells.Rh2 could inhibit the proliferation and migration, and induce apoptosis of daoy medulloblastoma cells through down‐regulation of mi r‐31 to inactivate the wnt/β‐catein signaling pathway.Therefore, rh2 may have a utility in clinical applications for the treatment of medulloblastoma.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-494 regulates Gli3 expression and inhibits pancreatic cancer cells growth and migration

Micro rna (mi r)‐494 has been identified as a predictor and inhibitor in pancreatic cancer.This study aimed to explore the role of mi r‐494 in pancreatic cancer cells, and the regulation of glioma‐associated oncogene 3 (gli3) by mi r‐494.The m rna level of gli3 in 99 pairs of pancreatic cancer and correspondingly adjacent tissues was monitored by q rt‐pcr.Correlation of gli3 expression with mi r‐494 level was assessed by pearson χ2 test.Dual‐luciferase reporter assay was used to detect whether gli3 was a target of mi r‐494.Following mi r‐494 mimics and mi r‐494 inhibitor transfection, the changes in cell viability and migration were detected by using cck‐8 and transwell chamber.Furthermore, gli3 si rna was co‐transfected with mi r‐494 inhibitor, and then cell viability and migration were redetected.Result showed that, the m rna level of gli3 in tumor tissues was higher than in the adjacent tissues ( p &lt; 0.01).There were 45 in 99 patients with pancreatic cancer expressed gli3, and significant correlations were observed between the gli3 level and vascular invasion ( p = 0.04), distant metastasis ( p = 0.001), and histologic grade ( p = 0.03).Gli3 was a direct target of mi r‐494 ( p &lt; 0.01) and it was negatively related by mi r‐494 ( p &lt; 0.01).Overexpression of mi r‐494 suppressed panc‐1 cells viability ( p &lt; 0.05, p &lt; 0.01, or p &lt; 0.001) and migration ( p &lt; 0.01).Additionally, gli3 silence suppresses mi r‐494 suppression‐induced cell viability and migration ( p &lt; 0.01).In conclusion, these data demonstrate mi r‐494 exhibits tumor‐suppressive effects on pancreatic cancer, possibly via targeting gli3.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Effects and mechanism of puerarin on the human retinoblastoma cells

Puerarin is an isoflavonoid that is extracted from kudzu root and is considered to have an anti‐tumor effect.In the present study, the effects of puerarin on human retinoblastoma (rb) cells and the related pathways was determined.The retinoblastoma rb cell lines were used in this study.Cell viability and colony formation capacity were measured by mtt and colony formation assays.Cell cycle was determined by flow cytometry.Cell migration and invasion were examined by transwell assay.The expression of cell cycle, emt, and mapk/erk signal pathway‐related proteins were detected by western blot following puerarin treatment.The results revealed that cell viability and proliferation of rb cells treated with puerarin were significantly lower in rb cells compared to the control group.Puerarin significantly decreased the proportion of cells during s phase which was accompanied with increase in cells at g0/1 and g2 phases.Moreover, puerarin suppressed cell migration, invasion and up‐regulated e‐cadherin expression as well as down‐regulated vimentin and α‐sma expression.Furthermore, puerarin treatment suppressed the expression of p‐mek and p‐erk in rb cells.Our findings suggest that puerarin contributes to in the treatment of rb and other malignant tumors.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression

This study aimed to investigate the effect and underlying mechanism of lnc rna awpph in bladder cancer (bc).A total of 20 ta‐t1 stage bc tissues, 20 t2‐t4 stage bc tissues, and 20 normal bladder tissues, as well as human bladder epithelial cell line sv‐huc‐1, human bc cell lines rt4, and t24 were obtained to detect the levels of awpph, enhancer of zeste homolog 2 (ezh2) and smad4 using rt‐q pcr or western blotting.Rt4 cells were transfected with pc‐awpph, pc‐ezh2, or pc‐control and t24 cells were transfected with si‐awpph, si‐ezh2, si‐control, or pc‐awpph + pc‐smad4, respectively.Then, cell proliferation, apoptosis, autophagy, and migration, were detected using mtt assay, colony formation assay, annexin v‐fitc/pi method, western blotting, and transwell analysis, respectively.The relationship of awpph and ezh2 or smad4 was evaluated by rna immunoprecipitation (rip) assay or chromatin immunoprecipitation (ch ip) assay.Compared with normal bladder tissues or cells, the levels of awpph and ezh2 were overexpressed, while smad4 was down‐regulated in bc tissues or cells (all p &lt; 0.01).Cell viability, colony number, and migration were significantly increased, while cell apoptosis ratio was reduced in cells with pc‐awpph compared with cells with pc‐control (all p &lt; 0.05), meanwhile, these effects were reversed by the treatment of pc‐smad4.Then, rip assay revealed that awpph could bind to ezh2 and ch ip assay showed smad4 was regulated by ezh2.Lnc rna awpph can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in bc by inhibiting smad4 via ezh2.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Suppression of long non-coding RNA LET potentiates bone marrow-derived mesenchymal stem cells (BMSCs) proliferation by upregulating TGF-β1

Long non coding rnas (lnc rnas) show an encouraging trend in regulating the proliferation of bone marrow‐derived mesenchymal stromal cells (bmscs).The present study investigated the role of lnc rna low expression in tumor (let) in bmscs proliferation.Our result showed that let was down‐regulated in rapidly proliferated bmscs ( p &lt; 0.05).Suppression of let promoted bmscs proliferation and over‐expression of let inhibited bmscs proliferation ( p &lt; 0.05).Let negatively regulated the expression of transforming growth factor β1 (tgf‐β1) in bmscs ( p &lt; 0.05).Knockdown of tgf‐β1 reversed the let suppression‐induced bmscs proliferation ( p &lt; 0.05).Moreover, knockdown of tgf‐β1 alleviated the let suppression‐induced activation of wnt/β‐catenin pathway in bmscs.Therefore, we drew the conclusion that let suppression promoted bmscs proliferation by up‐regulating the expression of tgf‐β1 and activating wnt/β‐catenin pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Knockdown of long non-coding RNA MALAT1 inhibits growth and motility of human hepatoma cells via modulation of miR-195

The metastasis‐associated lung adenocarcinoma transcription 1 (malat1) is a long non‐coding rna (lnc rna), exerts oncogenic role in multiple cancers, including hepatocellular carcinoma (hcc).This study was aimed to investigate its posttranscriptional regulation in hcc cells.Rt‐pcr was performed to monitor the expression levels of malat1 in normal liver and hcc cell lines.The expression of malat1, micro rna (mi r)‐195, and epidermal growth factor receptor (egfr) in hep g2 and mhcc97 cells was respectively or synchronously altered by transfection.Then the changes in cell viability, apoptotic cell rate, cell cycle distribution, migration, and invasion were respectively assessed.As a result, we found that malat1 was highly expressed in hcc cell lines when compared to normal liver cells.Malat1 silence suppressed hcc cells viability, migration and invasion, induced apoptosis, and arrested more cells in g0/g1 phase.Malat1 acted as a circular endogenous rna (ce rna) for mi r‐195.Malat1 silence could not suppress hcc cell growth and motility when mi r‐195 was knocked down.Egfr was a direct target of mi r‐195.Mi r‐195 overexpression could not suppress hcc cell growth and motility when the 3′utr site of egfr was overexpressed.Furthermore, malat1 silence blocked the activation of pi3k/akt and jak/stat pathways, while egfr overexpression activated them.Our study demonstrates malat1‐mi r‐195‐egfr axis plays a critical role in hcc cells which provided a better understanding of malat1 in hcc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Down-regulation of XIAP enhances the radiosensitivity of esophageal cancer cells in vivo and in vitro

The study investigated the effects of x-chromosome-linked inhibitor of apoptosis (xiap) gene silencing on the radiosensitivity of esophageal cancer (ec) cells.Western blotting was used to select ec cell lines with xiap overexpression.Selected ec9706 and kyse30 cell lines were both divided into four groups: the blank control group, the negative control (nc) group (transfected with p bshh1), the si rna-enhanced group (transfected with p bshh1-xiap1-si rna), and the si rna-decreased group (transfected with p bshh1-xiap2-si rna).Expressions of xiap were measured by reverse-transcription quantitative pcr (rt-q pcr) and western blotting, cell survival and viability by mtt assay and colony formation assay, and cell apoptosis by flow cytometry, respectively.Caspase-3 and caspase-9 activity were detected using caspase-3 and caspase-9 activity detection kits.A nude mice model of ec9706 cell line was established to measure tumorigenesis ability.Compared with the nc group, xiap m rna and protein expressions were decreased, caspase-3 and caspase-9 activity and apoptosis were up-regulated, and cell survival rate and colony-forming efficiency were lower in the si rna-enhanced and si rna-decreased groups in both the cell lines; while the opposite trends were found in the si rna-decreased group compared with the si rna-enhanced group.Tumor weight and volume of nude mice were decreased in the si rna-enhanced and si rna-decreased groups than those in the nc group, and were elevated in the si rna-decreased group compared with the si rna-enhanced group.These results indicate that xiap gene silencing would strengthen the radiosensitivity of ec9706 cells, which provides a novel target for the treatment of ec.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
microRNA-98 inhibits the proliferation, invasion, migration and promotes apoptosis of breast cancer cells by binding to HMGA2

Breast cancer is a major contributor leading to cancer death in females worldwide.The aim of the present study was to investigate the effects of micro rna-98 (mi r-98) on the processes of cell proliferation, invasion, migration and apoptosis by binding to high-mobility group at-hook 2 (hmga2) in breast cancer.Breast cancer tissues and adjacent normal tissues were collected from 112 patients suffering from breast cancer.The target relationship between mi r-98 and hmga2 was verified by in connection with the bioinformatics website as well as a dual-luciferase reporter assay, both of which provided evidence indicating that hmga2 was a target gene of mi r-98.Human breast cancer mda-mb-231 cells were treated with mi r-98 mimics, mi r-98 inhibitors, si rna-hmga2 or mi r-98 inhibitors + si rna-hmga2.3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry methods were performed to determine cell proliferation, cell cycle and apoptosis, respectively, while a transwell assay was employed to detect cell migration and invasion.Breast cancer tissues exhibited decreased mi r-98 expression, while increased expression levels of hmga2 were recorded.The m rna and protein expressions of hmga2, cell proliferation, cells at the s phase, cell migration, invasion, expressions of matrix metalloproteinase (mmp)2 as well as mmp9 were all reduced in response to mi r-98 mimics or si rna-hmga2, while a contradictory trend was observed in the mi r-98 inhibitors group.In conclusion, the results of the study demonstrate that mi r-98 inhibits cell proliferation, migration and invasion, while acting to promote apoptosis by negatively regulating hmga2 in breast cancer.

Journal: Bioscience Reports (2018)
Publication types: Research Article;
Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p

The study evaluated the ability of long intergenic noncoding rna linc00312 (linc00312) to influence the proliferation, invasion, and migration of thyroid cancer (tc) cells by regulating mi rna-197-3p.Tc tissues and adjacent normal tissues were collected from 211 tc patients.K1 (papillary tc), sw579 (squamous tc), and 8505c (anaplastic tc) cell lines were assigned into a blank, negative control (nc), linc00312 overexpression, mi r-197-3p inhibitors, and linc00312 overexpression + mi r-197-3p mimics group.The expression of linc00312, mi r-197-3p, and p120 were measured using quantitative real-time pcr (q rt-pcr) and western blotting.Cell proliferation was assessed via cck8 assay, cell invasion through the scratch test, and cell migration via transwell assay.In comparison with adjacent normal tissues, the expression of linc00312 is down-regulated and the expression of mi r-197-3p is up-regulated in tc tissues.The dual luciferase reporter gene assay confirmed that p120 is a target of mi r-197-3p.The expression of linc00312 and p120 was higher in the linc00312 overexpression group than in the blank and nv groups.However, the expression of mi r-197-3p was lower in the linc00312 overexpression group than in the blank and nc groups.The mi r-197-3p inhibitors group had a higher expression of mi r-197-3p, but a lower expression of p120 than the blank and nc groups.The linc00312 overexpression and mi r-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and nc groups.These results indicate that a linc00312 overexpression inhibits the proliferation, invasion, and migration of tc cells and that this can be achieved by down-regulating mi r-197-3p.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
HOTAIR contributes to cell proliferation and metastasis of cervical cancer via targeting miR-23b/MAPK1 axis

The long non-coding rna (lnc rna) hox transcript antisense rna (hotair) has been found to be overexpressed in many human malignancies and involved in tumor progression and metastasis.Although the downstream target through which hotair modulates tumor metastasis is not well-known, evidence suggests that mi r-23b might be involved in this event.In the present study, the expressions of hotair and mi r-23b were detected by real-time pcr in 33 paired cervical cancer tissue samples and cervical cell lines.The effects of hotair on the expressions of mi r-23b and mitogen-activated protein kinase 1 (mapk1) were studied by overexpression and rnai approaches.We found that hotair expression was significantly increased in cervical cancer cells and tissues.In contrast, the expression of mi r-23b was obviously decreased.We further demonstrated that hotair knockdown promoted apoptosis and inhibited cell proliferation and invasion in vitro and in vivo.Moreover, our data indicated that hotair may competitively bind mi r-23b and modulate the expression of mapk1 indirectly in cervical cancer cells.Taken together, our study has identified a novel pathway through which hotair exerts its oncogenic role, and provided a molecular basis for potential applications of hotair in the prognosis and treatment of cervical cancer.

Journal: Bioscience Reports (2018)
Publication types: Research Article;