syedzayyan/paper_mill_benchmark huggingface dataset:
Protective impacts of long noncoding RNA taurine-upregulated 1 against lipopolysaccharide-evoked injury in MRC-5 cells through inhibition of microRNA-127

Background pneumonia is a respiratory disease, which is triggered by pathogenic microorganisms or physical/chemical factors.Increasing evidence confirmed the vital impacts of long noncoding rnas on various inflammatory diseases.Nonetheless, the influence of taurine‐upregulated 1 (tug1) in pneumonia remains vague.The research tried to disclose the protective impacts of tug1 against lipopolysaccharide (lps)‐evoked injury in mrc‐5 cells.Methods mrc‐5 cells were disposed with lps to construct pulmonary injury model.Then, pc‐tug1 vector was transfected into mrc‐5 cells and the influence of overexpressed tug1 in cell viability, apoptosis, and pro‐inflammatory cytokines in lps‐disposed cells were evaluated.The correlation between tug1 and micro rna (mi r)−127 was estimated via utilizing real‐time quantitative polymerase chain reaction (rt‐q pcr), meanwhile whether mi r‐127 affected the impacts of tug1 on lps‐injured mrc‐5 cells was explored.Besides, nf‐κb and p38mapk pathways were evaluated to understand the dormant mechanisms.Results lps administration apparently evoked inflammatory injury in mrc‐5 cells by restraining cell viability, accelerating apoptosis, and enhancing tnf‐α and il‐6 productions.But, tug1 lightened lps‐evoked pro‐inflammatory response in mrc‐5 cells.In addition, mi r‐127 was repressed by overexpressed tug1, meanwhile the protective impacts of tug1 against lps‐evoked inflammatory injury in mrc‐5 cells were overturned by overexpressed mi r‐127.Finally, we disclosed that tug1 hindered the activation of nf‐κb and p38mapk pathways via restraining mi r‐127.Conclusions these explorations testified that taurine‐upregulated 1 (tug1) protected mrc‐5 cells against lipopolysaccharide (lps)‐evoked inflammatory injury via hindering mi r‐127/nf‐κb/p38mapk axis.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Sapylin inhibits lung cancer cell proliferation and promotes apoptosis by attenuating PI3K/AKT signaling

Sapylin (ok‐432) revealed biological properties in cancers.In this study, the effect of sapylin on lung cancer cell a549 was investigated.A549 cell lines were treated with sapylin (0.1, 0.5, and 1 ke/m l) for different time intervals.A549 cell proliferation and apoptosis was determined using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2h‐tetrazolium bromide/ki67 assay and flow cytometry, respectively.Western blot was used to determine the expressions of proteins involved in proliferation, apoptosis, and phosphoinositide 3‐kinase/serine/threonine kinase (pi3k/akt), wnt3a/β‐catenin signaling pathway.Level of intracellular reactive oxygen species (ros) was insured by using the ros kit.Sapylin inhibited a549 cell viability and the expressions of proliferation‐related proteins (cyclin e1 and d1) in dose‐ and time‐dependent manners.Sapylin promoted apoptosis in a dose‐ and time‐dependent manners.Sapylin also promoted the expressions of apoptotic proteins (cleaved caspase‐3 and 8) in dose‐ and time‐dependent manners.Furthermore, sapylin increased the intracellular concentration of ros in a dose‐dependent manner.Besides, the high expression of ros level might induce inhibition of cell viability and increase cell apoptosis.The mechanistic study revealed that sapylin inactivated the pi3k/akt and wnt3a/β‐catenin signaling pathways.Our findings suggest that sapylin inhibits proliferation and promotes apoptosis in lung cancer cells, thus providing a new theoretical basis for the treatment of lung cancer.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
lncRNA-ATB promotes viability, migration, and angiogenesis in human microvascular endothelial cells by sponging microRNA-195

The atherosclerosis in the arterial system of the extremities is considered as the major pathogenesis of peripheral arterial disease.The present work aimed to explore the potential role of long noncoding rna activated by tumor growth factor‐β (lnc rna‐atb) on the dysfunction of endothelial cells.Human microvascular endothelial cells (hmec‐1) were transfected with lnc rna‐atb expressing vectors, and then the formation of tubes and expression of proteins associated with angiogenesis were analyzed using microscope and reverse transcription‐quantitative polymerase chain reaction (rt‐q pcr)/western blot analysis.Cell viability, migration, and micro rna‐195 (mi r‐195) expression were examined by cell counting kit‐8 assay, modified boyden chambers, western blot analysis, and rt‐q pcr.The interaction between lnc rna‐atb and mi r‐195 was determined by rt‐q pcr, dual‐luciferase reporter assay, and biotin‐avidin pull‐down assay.Finally, expression of key kinases in the pi3k/akt and mek/erk pathways was determined by western blot analysis.We found vascular tubulogenesis was induced spontaneously when hmec‐1 cells were cultured in matrigel‐coated plates.Lnc rna‐atb overexpression increased cell viability, migration and formation of tubes, along with upregulation of matrix metalloproteinase‐2 (mmp‐2), mmp‐9, and vascular endothelial growth factor.Then, we found lnc rna‐atb worked as a molecular sponge for mi r‐195, and the effects of lnc rna‐atb on hmec‐1 cells were reversed by mi r‐195 overexpression while were augmented by mi r‐195 inhibition.Phosphorylated levels of key kinases in the pi3k/akt and mek/erk pathways were increased by lnc rna‐atb via mi r‐195.In conclusion, lnc rna‐atb enhanced cell viability, migration and angiogenesis in hmec‐1 cells through sponging mi r‐195.Moreover, the pi3k/akt and mek/erk pathways were activated by lnc rna‐atb via mi r‐195.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Vinculin promotes gastric cancer proliferation and migration and predicts poor prognosis in patients with gastric cancer

Vinculin is a highly conserved protein involved in cell proliferation, migration, and adhesion.However, the effects of vinculin on gastric cancer (gc) remain unclear.Therefore, we aimed to explore the functional role of vinculin in gc, as well as its underlying mechanism.Expression of vinculin in patients with gc was analyzed by real‐time polymerase chain reaction, western blot analysis, and immunohistochemistry.Overall survival was evaluated by the kaplan‐meier method with the log‐rank test.The relationship between vinculin and clinicopathological characteristics of patients with gc was further identified.In addition, we assessed the expression of vinculin in gc cell lines.Besides, vinculin was suppressed or overexpressed by transfection with small interfering (si‐vinculin) or pc dna‐vinculin and then cell viability, cell apoptosis, and/or migration was respectively examined by the 3‐(4, 5‐dimethylthiazole‐2‐yl)‐2, 5‐biphenyl tetrazolium bromide assay, flow cytometer, and scratch assay, respectively.Moreover, the cell cycle‐ and apoptosis‐related proteins were detected by western blot analysis.The expression of vinculin was significantly increased in the gc tissues and cells compared with the nontumor tissues or cells.Vinculin protein positive staining was mainly located in the cell membrane and cytoplasm.Moreover, vinculin was significantly associated with tumor node metastasis (tnm) and poor differentiation.Patients with high vinculin levels had significantly worse overall survival than those with low levels.Suppression of vinculin significantly decreased cell viability and migration and promoted cell apoptosis.However, overexpression of vinculin statistically increased cell viability but had no effects on cell apoptosis.Vinculin promotes gc proliferation and migration and predicts poor prognosis in patients with gc.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Upregulation of long noncoding RNA TUG1 contributes to the development of laryngocarcinoma by targeting miR-145-5p/ROCK1 axis

Laryngocarcinoma is the most common head and neck cancer and has a high incidence and mortality, causing about 83 000 deaths per year worldwide.Our research aimed to investigate the possible role of long noncoding rna (lnc rna) taurine upregulated gene 1 (tug1) in laryngocarcinoma development.The messenger rna (m rna) levels of tug1 in tumor tissues and control (plasma) samples of laryngocarcinoma patients as well as in laryngocarcinoma cells were detected.The influences of tug1 suppression on cell biological processes (viability, apoptosis, migration, and invasion) and cytoskeleton rearrangement in laryngocarcinoma cells were tested.Moreover, we investigated the regulatory interaction between tug1 and mi r‐145‐5p, and identified the target gene of mi r‐145‐5p.The association between tug1 and the protein expressions of rho a/rho associated coiled‐coil containing protein kinase (rock)/matrix metalloproteinases (mmps) pathway‐associated factors were detected.Tug1 was found to be highly expressed in tumor tissues and plasma samples of laryngocarcinoma patients as well as in laryngocarcinoma cells.Suppression of tug1 decreased laryngocarcinoma cell viability, increased apoptosis, and suppression migration, invasion, and cytoskeleton rearrangement.Moreover, tug1 negatively regulated mi r‐145‐5p.Tug1 regulated tumor growth (viability and apoptosis) and metastasis through mi r‐145‐5p.Furthermore, rock1 was targeted by mi r‐145‐5p, and mi r‐145‐5p/rock1 partner was involved in the process of tumor growth and metastasis.Finally, we found that tug1 functioned on laryngocarcinoma by activating rho a/rock/mmps pathway.Our study reveals that lnc rna tug1 is upregulated in laryngocarcinoma and may be involved in the process of laryngocarcinoma through mi r‐145‐5p downregulation and activating the rho a/rock/mmps signals.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
The long noncoding RNA cardiac hypertrophy-related factor plays oncogenic roles in hepatocellular carcinoma by downregulating microRNA-211

Background hepatocellular carcinoma (hcc) is the most major type of primary hepatic cancer.This study aimed to explore the possible oncogenic effects of the long noncoding rna cardiac hypertrophy–related factor (chrf) on hcc, as well as the underlying possible mechanism.Methods the expression levels of chrf and micro rna‐211 (mi r‐211) in hcc tissues and/or cell lines hep g2 and huh‐7 were measured using quantitative reverse transcription polymerase chain reaction.Cell transfection was conducted to change the expression levels of chrf and mi r‐211 in cells.Cell viability and apoptosis were assessed using the cell counting kit‐8 assay and annexin v‐phycoerythrin staining, respectively.The pull‐down assay and rna immunoprecipitation were performed to analyze the association between chrf and mi r‐211.The expression of the key factors involving in cell proliferation, cell apoptosis, and epithelial‐mesenchymal transition (emt) process, as well as the phosphoinositide‐3‐kinase (pi3k)/protein kinase b (akt) and wnt/β‐catenin pathways, were evaluated by western blot analysis.Results chrf was highly expressed in hcc tissues and positively associated with the tnm stage, differentiation, and size of tumors.Overexpression of chrf promoted hep g2 cell viability, proliferation, and emt process.Chrf knockdown had opposite effects.Moreover, chrf negatively regulated the expression of mi r‐21, and mi r‐21 was a direct target of chrf.Overexpression of mi r‐211 reversed the effects of chrf on hep g2 and huh‐7 cell viability, proliferation, and emt process.Furthermore, overexpression of chrf activated the pi3k/akt and wnt/β‐catenin pathways in hep g2 cells by downregulating mi r‐211.Conclusion chrf played oncogenic roles in hcc.The overexpression of chrf promoted hep g2 and huh‐7 cell viability, proliferation, and emt process by downregulating mi r‐211 and then activating the pi3k/akt and wnt/β‐catenin pathways.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
HOXA3 promotes tumor growth of human colon cancer through activating EGFR/Ras/Raf/MEK/ERK signaling pathway

Homeobox a3 (hoxa3), one of hox transcription factors, regulates gene expression during embryonic development.Hoxa3 expression has been reported to be associated with several cancers; however, its role in colon cancer and underlying mechanism are still unclear.The expression of hoxa3 in 232 paired of human colon tumor and adjacent non‐tumorous tissues were measured by q pcr.The relationship between hoxa3 expression and clinical outcomes were analyzed by kaplan‐meier survival curves analysis.Human colon cancer cell lines ht29 and htc116 were transfected with hoxa3 si rna, or hoxa3 expressing vector, and then cell proliferation and apoptosis were assessed, respectively.Western blot was performed to detect the activation of egfr/ras/raf/mek/erk signaling pathway.Moreover, hoxa3‐overexpressing and hoxa3‐suppressing ht29 cells were subcutaneous injected into nod mice to confirm the regulation of hoxa3 on egfr/ras/raf/mek/erk signaling in regulating tumor growth.Hoxa3 was upregulated in colon tumor tissues and cell lines, and upregulated expression of hoxa3 was associated with low survival rate.Knockdown of hoxa3 suppressed cell viability and clone formation, while induced cell apoptosis.Hoxa3 knockdown could not induce the increase of cell apoptosis on the condition of egfr overexpression.In vivo xenograft studies, hoxa3‐suppressing cells showed less tumorigenic.Moreover, hoxa3 knockdown suppressed the activation of egfr/ras/raf/mek/erk signaling pathway.To conclude, this study indicated that hoxa3 might act as a promoter of human colon cancer formation by regulating egfr/ras/raf/mek/erk signaling pathway.Hoxa3 might be a potential therapeutic target for the treatment of colon cancer.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
MicroRNA-29a inhibits proliferation and motility of schwannoma cells by targeting CDK6

Micro rna‐29 (mi r‐29) family is involved in various types of cancer regulation.Although mi r‐29 family was shown to play an inhibitory role in tumorigenesis, the effect of mi r‐29a expression on schwannoma cells still remains unclear.In this study, we aimed to explore the role of mi r‐29 family in schwannoma.The expressions of mi r‐29a, mi r‐29b, and mi r‐29c were detected in the schwann tissues and cell lines using q rt‐pcr.The effect of mi r‐29a, mi r‐29b, and mi r‐29c on cell viability, migration, invasion, and apoptosis was tested.Then, the regulatory relationship between mi r‐29a and ckd6 was detected using q rt‐pcr, western blot, and luciferase assay.Finally, the phosphorylation levels of mainly factors in jnk and p38mapk/erk pathways were analyzed by western blot.The expression of mi r‐29a, mi r‐29b, and mi r‐29c was downregulated in schwann tissues and cell lines.Cell viability, migration, invasion were decreased, while apoptosis was increased when mi r‐29a, mi r‐29b, and mi r‐29c overexpression.We further found that mi r‐29a negatively regulated expression of cdk6.Then, knockdown of mi r‐29a promoted cell viability, migration, invasion, and inhibited apoptosis in schwannoma cells by upregulating cdk6 expression.In addition, the overexpression of mi r‐29a downregulated cdk6 expression by deactivation of jnk and p38mapk/erk pathways.Our data suggested that mi r‐29a could play an important role in inhibiting proliferation and motility of cancerous schwann cells, and may suppress tumor growth through upregulation of cdk6.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Knockdown of long non-coding RNA MEG3 protects H9c2 cells from hypoxia-induced injury by targeting microRNA-183

Acute myocardial infarction (ami) occurs when blood supply to the heart is diminished (ischemia) for long time, and ischemia is primarily caused due to hypoxia.This study evaluated the effects of long non‐coding rna maternally expressed gene 3 (meg3) on hypoxic rat cardiomyocyte‐drived h9c2 cells.Hypoxic injury was confirmed by alterations of cell viability, migration, invasion, apoptosis, and hypoxia‐inducible factor 1α (hif‐1α) expression.Meg3 level in hypoxic cells and effects of its knockdown on hypoxic cells were assessed.The interactions between meg3 and mi r‐183 as well as mi r‐183 and p27 were investigated.In addition, the effects of aberrantly expressed meg3, mi r‐183, and p27 on hypoxic cells along with the activation of pi3k/akt/foxo3a signaling pathway were all assessed.Results showed that hypoxia induced decreases of cell viability, migration and invasion, and increases of apoptosis and expressions of hif‐1α and meg3.Knockdown of meg3 decreased hypoxia‐induced injury in h9c2 cells.Knockdown of meg3 also increased mi r‐183 expression, which was identified as a target of meg3.The effects of meg3 knockdown on the hypoxic cells were reversed by mi r‐183 silence.P27 was identified as a target gene of mi r‐183, and its expression negatively regulated by mi r‐183.The mechanistic studies revealed that knockdown of p27 decreased hypoxia‐induced h9c2 cell injury by activating pi3k/akt/foxo3a signal pathways.These findings suggest that knockdown of meg3 alleviates hypoxia‐induced h9c2 cell injury by mi r‐183‐mediated suppression of p27 through activation of pi3k/akt/foxo3a signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Knockdown of lncRNA MEG3 inhibits viability, migration, and invasion and promotes apoptosis by sponging miR-127 in osteosarcoma cell

Osteosarcoma (os) is one of the most common bone malignancies and occurs almost exclusively in children and adolescents.This study aimed to explore the role of lnc rna maternally expressed gene 3 (meg3) in os cells growth and metastasis, and to uncover the possible underlying mechanism.In this study, the expressions of meg3 in five os cell lines (mg63, os‐732, sa os, g292, and 143b) and in a human osteoblast cell line h fob1.19 were measured by q rt‐pcr analysis.The expressions of meg3, mi r‐127, and zeb1 in os‐732 cells were overexpressed or suppressed by transfection.Cell viability, migration, invasion, and apoptosis were then assessed.The results showed that meg3 was highly expressed in os cell lines when compared to h fob1.19 cell.Meg3 silence significantly suppressed os‐732 cells growth and metastasis, as evidenced by the decreases in cell viability, migration, invasion, and increase in apoptotic cell rate.Meg3 acted as an endogenous sponge by binding to mi r‐127.More interestingly, meg3 silence could not suppress os‐732 cells growth and metastasis when mi r‐127 was knocked down.Zeb1 was a target gene of mi r‐127, and mi r‐127 overexpression‐induced impairments in cell growth and metastasis were attenuated when zeb1 was overexpressed.Moreover,mi r‐127 suppression activated jnk and wnt signaling pathways, while these activations were recovered by zeb1 silence.To conclude, our findings suggest that lnc rna meg3 promoted os cells growth and metastasis in vitro through sponging mi r‐127.This study provides the evidence that meg3 may be a potential therapeutic target for os.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
LncRNA-LET relieves hypoxia-induced injury in H9c2 cells through regulation of miR-138

Ischemic heart disease (ihd) is a common cardiovascular disease, occurs when coronary artery blood circularity cannot match with the heart's need.The present work attempted to study the effects of long noncoding rna (lnc rna) low expression in tumor (let) on the progression of ihd.H9c2 cells were injured by hypoxia to mimic a cell model of ihd.The effects of lnc rna‐let on hypoxia‐injured h9c2 cells were tested by using cell counting kit‐8 assay, flow cytometry, and western blot analysis.Micro rna‐138 (mi r‐138) expression was tested by a quantitative real‐time polymerase chain reaction, and the expression of c‐jun n‐terminal kinase (jnk) and p38mapk (p38–mitogen‐activated protein kinase) proteins was measured by western blot analysis.We found that hypoxia exposure significantly repressed the viability of h9c2 cells, and induced apoptosis.Meanwhile, phosphorylation of jnk and p38mapk was enhanced by hypoxia.The expression of lnc rna‐let was repressed by hypoxia.Overexpression of lnc rna‐let attenuated hypoxia‐induced injury in h9c2 cells.Moreover, mi r‐138 was a downstream effector of lnc rna‐let, that mi r‐138 was highly expressed in lnc rna‐let‐overexpressed cell.The cardioprotective effects of lnc rna‐let were abolished when mi r‐138 was silenced.In conclusion, this study revealed the cardioprotective function of lnc rna‐let.Lnc rna‐let conferred its cardioprotective effects possibly via upregulation of mi r‐138 and thus repressing the jnk and p38mapk pathways.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Silence of lncRNA HEIH suppressed liver cancer cell growth and metastasis through miR-199a-3p/mTOR axis

Background/aims high expression in hepatocellular carcinoma (heih) is an long noncoding rna (lnc rna) which is highly expressed in hepatocellular carcinoma (hcc).Aberrant expression of heih is implicated in regulating hcc cells growth and metastasis.This study attempted to illustrate the effects of heih on hcc cell lines.Methods the expression changes of heih in hcc tumor tissues and the paracancerous tissues derived from 20 patients with hcc were tested.Effects of heih on huh7 and hep3b cells viability, apoptosis, migration, and invasion were assessed by silencing heih in vitro.Furthermore, downstream effector and signaling of heih were studied.Results as compared with the paracancerous tissues, the heih expression was highly expressed in tumor tissues.Silence of heih significantly reduced huh7 and hep3b cells viability, migration, and invasion, but induced apoptosis.It was coupled with the downregulated cyclin d1, bcl‐2, mmp‐2, mmp‐8, vimentin, the upregulated p53, bax, as well as the cleaved caspase‐3.Micro rna (mi r)‐199a‐3p was identified as a downstream effector of heih, as its expression was upregulated by heih silence, and the functional effects of heih on huh7 and hep3b cells were all attenuated when mi r‐199a‐3p expression was suppressed.Furthermore, heih silence suppressed the activation of m tor signaling via upregulating mi r‐199a‐3p.Conclusion heih silence might be a promising target for suppressing hcc cells growth and metastasis.Silence of heih exerted its antitumor properties possibly through upregulating mi r‐199a‐3p, and thereby blockage of m tor signaling.

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