syedzayyan/paper_mill_benchmark huggingface dataset:
Long noncoding RNA Alu-mediated p21 transcriptional regulator promotes proliferation, migration, and pipe-formation of human microvascular endothelial cells by sponging miR-126

Peripheral artery disease (pad) is a serious hazard to the elderly in the lower extremity atherosclerotic plaque, accompanied by a large number of angiogenesis.Long noncoding rna alu‐mediated p21 transcriptional regulator (aptr) exerts important functions in promoting cell growth.Therefore, we planned to research the mechanism of aptr in angiogenesis in pad.Cck‐8 assay, flow cytometry analysis, and migration assay were to detect cell viability, apoptosis, and migration respectively.The interaction between aptr and mi r‐12 was tested through luciferase activity test.In vitro angiogenesis assay was used to test the number of tubular cells.Q rt‐pcr and western blot were to test expression of aptr, mi r‐126, and angiogenesis relative factors.There was spontaneously pipe‐formation in hemc‐1 cells under matrigel condition.Knockdown of aptr inhibited cell viability and migration and reduced the number of tubular cells.Further, aptr sponged mi r‐126 and downregulating mi r‐126 to promote angiogenesis.Overexpression of aptr promoted cell activity and migration and increased the number of tubular cells via negatively regulating mi r‐126.Aptr could elevate activating phosphatidylinositol 3 kinase/protein kinase b and mitogen extracellular kinase/extracellular signal‐regulated kinase signal pathways via negatively regulating mi r‐126 to promote cell proliferation, migration, and pipe‐formation.We researched the mechanism of angiogenesis that aptr elevated proliferation, migration, and pipe‐formation via negatively regulating mi r‐126.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Notoginsenoside R1 protects WI-38 cells against lipopolysaccharide-triggered injury via adjusting the miR-181a/TLR4 axis

Notoginsenoside r1 (ngr1) is a neoteric phytoestrogen extracted from panax notoginseng , and possesses comprehensive pharmacological functions in multitudinous ailments.But, whether ngr1 is utilized in neonatal pneumonia is not clear.This research study aspired to disclose the protective activity of ngr1 in neonatal pneumonia.Wi‐38 cells were co‐stimulated with ngr1 and lipopolysaccharide (lps, 10 ng/m l), cck‐8 and flow cytometry assays were implemented for cell viability and apoptosis assessment.Real‐time quantitative plymerase chain reaction (rt‐q pcr), enzyme‐linked immunosorbent assay (elisa), and western blot analysis were executed for inflammatory cytokine determination.Micro rna‐181a (mi r‐181a) expression was evaluated through rt‐q pcr, simultaneously, the impact of mi r‐181a was estimated in ngr1 and lps co‐managed cells.Dual luciferase report assay was performed to disclose the relation between mi r‐181a and toll‐like receptor 4 (tlr4).The nuclear factor‐κb (nf‐κb) and tak1/jnk pathways were ultimately appraised.We found that ngr1 decreased cell viability, evoked apoptosis and impeded interleukin‐1β (il‐1β), il‐6, and tumor necrosis factor‐α (tnf‐α) expression and secretions in lps‐managed wi‐38 cells.Mi r‐181a expression was enhanced by ngr1, and mi r‐181a inhibition inverted the impacts of ngr1 in lps‐managed wi‐38 cells.Besides, tlr4 was predicted to be a firsthand direct target of mi r‐181a.Furthermore, ngr1 hindered nf‐κb and tak1/jnk pathways through modulating tlr4.These discoveries disclosed the fact that ngr1 protected wi‐38 cells against lps‐triggered injury via adjusting the mi r‐181a/tlr4 and nf‐κb and tak1/jnk pathways.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Knockdown of lncRNA-UCA1 inhibits cell viability and migration of human glioma cells by miR-193a-mediated downregulation of CDK6

Background long noncoding rna urothelial carcinoma‐associated 1 (lnc rna‐uca1) is generally recognized as an oncogenic molecule in several human malignant tumors.However, the available evidence does not necessarily imply an unequivocal causal function of uca1 in glioblastoma.The current study was aimed to probe the biological function of lnc rna‐uca1 in human glioblastoma cell lines.Besides, we further investigated the potential mechanisms.Methods cell viability, apoptosis, as well as migration and invasion were measured using a commercial cell counting kit‐8, flow cytometry, and 24‐transwell assay, respectively.Lnc rna‐uca1, micro rna‐193a (mi r‐193a), and cdk6 at messenger rna levels were evaluated by quantitative real‐time polymerase chain reaction method.Protein level was examined by western blot analysis.Rna immunoprecipitation was utilized to validate lnc rna‐uca1 associated with mi r‐193a.Luciferase activity assay was used to identify the mi r‐193a‐targeted cdk6 3′‐untranslated region.Results lnc rna‐uca1 knockdown weakened cell viability, augmented apoptosis progression, as well as suppressed migration and invasion behaviors in glioblastoma cells, whereas lnc rna‐uca1 silence exhibited the opposite functions.Lnc rna‐uca1 functioned as an endogenous sponge of mi r‐193a.Mi r‐193a silence reversed the biological function of lnc rna‐uca1 knockdown on u‐118 mg cells.Mi r‐193a negatively regulated the expression of cdk6, and it affected the u‐118 mg cells through regulating cdk6 expression.Cdk6 overexpression abrogated the blockage of pi3k/akt, mitogen‐activated protein kinase (mapk), and notch signaling pathways.Furthermore, lnc rna‐uca1 and mi r‐193a could affect these signaling cascades through regulating cdk6 expression.The regulatory mechanisms of lnc rna‐uca1 were further consolidated in clinical specimens.Conclusion lnc rna‐uca1 silence reduced cell viability, promoted apoptosis progression, while impeding the migration and invasion of glioblastoma cells by mi r‐193a‐mediated silence of cdk6, with blockage of pi3k/akt, mapk, and notch pathways.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Knockdown of long noncoding RNA HOTAIR inhibits cell growth of human lymphoma cells by upregulation of miR-148b

Lymphoma is a common cause of cancer worldwide with an increasing incidence in recent years.A large number of studies have shown that hox transcript antisense intergenic rna (hotair) exerts as an oncogene in various neoplasms.However, the function of hotair in lymphoma still remains unclear.The present study aimed to investigate the function of hotair in lymphoma and its underlying mechanisms.The expressions of hotair, mi r‐148b, and bmi1 in lymphoma samples and cells (ahh‐1, raji, and u937) were quantified by quantitative reverse polymerase chain reaction (q rt‐pcr).Cell viability was measured by trypan blue assay.The efficiency of transfection was verified by q rt‐pcr or western blot analysis.Apoptotic cells and cell cycle progression were both detected by flow cytometry assay.Furthermore, western blot analysis was performed to assess the expression of mitogen‐activated protein kinase (mapk) and extracellular signal‐regulated kinase (erk) pathway‐related core factors.We found that hotair knockdown reduced cell viability but increased apoptotic cells and inhibited cell cycle progression in raji and u937 cells.Mi r‐148b expression was upregulated by hotair inhibition.Meanwhile, mi r‐148b inhibitor abolished the modulation of hotair silence on cell growth, as evidenced by increased cell viability, reduced apoptotic cells, and decreased the rate of g1 phase cells.Furthermore, mi r‐148b negatively regulated the expression of bmi1 by targeting its 3′‐untranslated region (3′‐utr), and bmi1 overexpression blocked the effect of mi r‐148b mimic on cell growth.In addition, bmi1 promoted the activation of mapk and erk in raji and u937 cells.In conclusion, the present study demonstrated that hotair knockdown inhibited the cell growth and promoted apoptosis of lymphoma cells via upregulation of mi r‐148b and mi r‐148b further regulated the expression of bmi1 via mapk and erk signaling pathways.

Journal: Journal of Cellular Biochemistry (2019)
Publication types: Research Article;
Deletion of long noncoding RNA EFNA3 aggravates hypoxia-induced injury in PC-12 cells by upregulation of miR-101a

Long noncoding rnas (lnc rnas) have been reported to be involved in several neurological pathogenesis conditions including cerebral ischemia.In the current study, the functions of lnc rna efna3 on hypoxia‐injured rat adrenal pheochromocytoma (pc‐12) cells and the underlying molecular mechanism were studied.The expression of lnc rna efna3 was silenced by short hairpin rna transfection, after which the cells were subjected with hypoxia.Cell viability, migration, invasion, and apoptosis were, respectively, determined by trypan blue staining, transwell assay, annexin v‐fluorescein isothiocyanate (fitc)/propidium iodide (pi) double‐staining, and western blot analysis.The cross regulation between lnc rna efna3 and mi r‐101a, as well as between mi r‐101a and rho associated coiled‐coil containing protein kinase 2 (rock2) were detected by performing quantitative real‐time polymerase chain reaction, rna pull‐down, rna immunoprecipitation, luciferase activity assay, and western blot analysis.Studies showed that lnc rna efna3 was highly expressed in response to hypoxia.Deletion of lnc rna efna3 significantly aggravated hypoxia‐induced injury in pc‐12 cells, as the impairment of cell viability, migration, and invasion, and the inducement of apoptosis.Lnc rna efna3 worked as a sponging molecule for mi r‐101a and mi r‐101a suppression‐protected pc‐12 cells against hypoxia‐induced injury even when lnc rna efna3 was silenced.Rock2 was a target gene of mi r‐101a.Rock2 overexpression exhibited neuroprotective activities.Besides, rock2 overexpression activated wnt/β‐catenin pathway whereas it deactivated jak/stat pathway upon hypoxia.Our study suggests that deletion of lnc rna efna3 aggravates hypoxia‐induced injury in pc‐12 cells by upregulating mi r‐101a, which further targets rock2.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-133a inhibits gastric cancer cells growth, migration, and epithelial-mesenchymal transition process by targeting presenilin 1

Gastric cancer (gc) is one of the most common malignancies and a leading cause of cancer‐related death worldwide.Accumulating evidence reported that micro rna (mi r)‐133a was involved in gc.This study aimed to investigate the function and mechanism of mi r‐133a in the development and progression of gc.The expression of mi r‐133a and presenilin 1 (psen1) in two gc cell lines, sgc‐7901 and bgc‐823, were inhibited and overexpressed by transient transfections.Thereafter, cell viability, migration, and apoptosis were measured by trypan blue exclusion assay, transwell migration assay, and flow cytometry assay, respectively.Dual‐luciferase reporter assay was conducted to verify whether psen1 was a direct target of mi r‐133a.Furthermore, quantitative real‐time polymerase chain reaction and western blot analysis were mainly performed to assess the expression changes of epithelial‐mesenchymal transition (emt)‐associated proteins, apoptosis‐related proteins, and notch pathway proteins.Mi r‐133a inhibitor significantly increased cell viability and migration, while mi r‐133a mimic decreased cell viability, migration, and induced apoptosis.Mi r‐133a suppression accelerated transforming growth factor‐β1 (tgf‐β1)‐induce emt, as evidenced by upregulation of e‐cadherin, and downregulation of n‐cadherin, vimentin, and slug.Of contrast, mi r‐133a overexpression blocked tgf‐β1‐induce emt by altering these factors.Psen1 was a direct target of mi r‐133a, and suppression of psen1 abolished the promoting functions of mi r‐133 suppression on cell growth and metastasis.Moreover, psen1 inhibition decreased notch 1, notch 2, and notch 3 protein expressions.This study demonstrates an antigrowth and antimetastasis role of mi r‐133a in gc cells.Additionally, mi r‐133a acts as a tumor suppressor may be via targeting psen1.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Long noncoding RNA MALAT1 alleviates lipopolysaccharide-induced inflammatory injury by upregulating microRNA-19b in murine chondrogenic ATDC5 cells

Osteoarthritis is the most frequent chronic bone‐joint disease in middle‐aged and older people worldwide.This study investigated the effects of long noncoding rna metastasis‐associated lung adenocarcinoma transcript 1 (malat1) on lipopolysaccharide (lps)‐induced murine chondrogenic atdc5 cell inflammatory injury.Cell viability and apoptosis were assessed using cell counting kit‐8 assay and annexin v‐phycoerythrin (pe) staining, respectively.The expression levels of interleukin‐1β (il)‐1β, il‐6, il‐8, tumor necrosis factor α (tnf‐α), malat1, and micro rna‐19b (mi r)‐19b were measured using quantitative reverse‐transcription polymerase chain reaction.Enzyme‐linked immunosorbent assay was conducted to detect the concentrations of il‐1β, il‐6, il‐8, and tnf‐α in culture supernatant of atdc5 cells.Expressions of key factors involved in cell apoptosis, proinflammatory response, wnt/β‐catenin, and nuclear factor κb (nf‐κb) pathways were analyzed using western blot analysis.We found that lps treatment remarkably induced atdc5 cell apoptosis and inflammatory injury.Malat1 was upregulated in lps‐stimulated atdc5 cells.Overexpression of malat1 significantly reversed the lps‐induced atdc5 cell inflammatory injury, while suppression of malat1 had opposite effects.Further results showed that malat1 positively regulated the expression of mi r‐19b in atdc5 cells.Knockdown of mi r‐19b reversed the protective effect of malat1 on lps‐induced atdc5 cells.In addition, malat1 reduced lps‐induced wnt/β‐catenin and nf‐κb pathways activation in atdc5 cells by upregulating mi r‐19.To conclude, our research verified that malat1 alleviated lps‐induced atdc5 cell inflammatory injury by upregulating mi r‐19b and inactivating wnt/β‐catenin and nf‐κb pathways.This finding will be helpful for further understanding the critical roles of malat1 and mi r‐19b in osteoarthritis and may provide possible targets for osteoarthritis diagnosis and treatment.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
miR-145 eliminates lipopolysaccharides-induced inflammatory injury in human fibroblast-like synoviocyte MH7A cells

Recently, it has been accepted that mi r‐based therapy may be beneficial for rheumatoid arthritis (ra).This study aimed to evaluate the potential involvement of mi r‐145 in ra in vitro.The expression of mi r‐145 in the human fibroblast‐like synoviocyte line mh7a was overexpressed by mi r‐mimic transfection, after which cells were subjected to lipopolysaccharides (lps).Cell viability, apoptosis, and the release of pro‐inflammatory cytokines were measured.The result showed that the apoptosis and the release of il‐1β, il‐6, il‐8, and tnf‐α were significantly induced by lps.Meanwhile, lps treatment led to downregulation of mi r‐145.Mi r‐145 overexpression in lps‐untreated mh7a cells had no impacts on cell apoptosis and inflammation.But, restoring mi r‐145 expression in lps‐stimulated cells by supplementation of a mi r‐145 mimic protected mh7a cells against lps‐induced apoptosis and inflammation.Furthermore, mi r‐145 overexpression in lps‐untreated mh7a cells slightly blocked the pi3k/atk and m tor pathways, whereas mi r‐145 overexpression in lps‐stimulated cells notably repressed the lps‐induced activation of pi3k/atk and mapk/m tor pathways.Our study suggested that mi r‐145 protected mh7a cells against lps‐induced apoptosis and inflammation by inhibiting the pi3k/akt and mapk/m tor pathways.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
microRNA-590-5p targets transforming growth factor β1 to promote chondrocyte apoptosis and autophagy in response to mechanical pressure injury

This study aimed to investigate the role of mi r‐590‐5p in chondrocyte apoptosis and autophagy in response to mechanical pressure injury in vitro, as well as to elucidate its regulatory mechanism in the pathogenesis of osteoarthritis.We applied mechanical pressure of 10 mpa to chondrocytes for 60 minutes to establish the chondrocyte model of experimentally induced mechanical injury.We then investigated the expression of mi r‐590‐5p in the injury model and the effects of mi r‐590‐5p dysregulation on the expression of cell apoptosis–related and autophagy‐related proteins.Cell apoptosis was detected by flow cytometry.Moreover, the potential targets of mi r‐590‐5p were investigated.Mechanical pressure injury resulted in a significantly increased expression of mi r‐590‐5p.Suppression of mi r‐590‐5p significantly increased chondrocytes viability, inhibited chondrocytes apoptosis and autophagy in response to mechanical pressure injury.In addition, mechanical pressure injury led to a decreased expression of transforming growth factor β1 (tgfβ1).Moreover, tgfβ1 was confirmed as a direct target of mi r‐590‐5p.Knockdown of tgfβ1 significantly induced chondrocytes apoptosis and autophagy in response to mechanical pressure injury, which was contrary to the effects of mi r‐590‐5p suppression.Furthermore, overexpression of tgfβ1 and mi r‐590‐5p at the same time significantly reversed the effects of overexpression of mi r‐590‐5p alone on chondrocytes apoptosis and autophagy.Our results indicate that upregulation of mi r‐590‐5p may target tgfβ1 to promote chondrocyte apoptosis and autophagy in response to mechanical pressure injury, thus contributing to the pathogenesis of osteoarthritis.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway

Osteosarcoma (os) is an aggressive malignant tumor of bone, which often occurs in children and adolescents.Currently, the effective method for the treatment of os is still limited.The study aimed to investigate the synergistic antitumor effect of inositol polyphosphate‐4‐phosphatase, type‐ii (inpp4b) and rucaparib on os cells.The expression levels of inpp4b in os tissues and os cell lines were examined by quantitative real‐time polymerase chain reaction and western blot analysis.Sa os2 and u2os cells were then transfected with overexpression vector of inpp4b or were treated with different concentrations of rucaparib, and cell viability, cell cycle, and apoptosis were determined by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide and flow cytometry.Western blot assay uncovered the combined effects of inpp4b and rucaparib on cell cycle, apoptosis and phosphoinositide 3‐kinase/protein kinase b (pi3k/akt) signal pathway.Further, the tumor formation was examined in vivo.Results showed that inpp4b was low expressed in os tissues and in os cell lines.Inpp4b overexpression significantly decreased cell viability and induced apoptosis in sa os2 and u2os cells.Additionally, rucaparib remarkably reduced cell viability in a dose‐dependent and time‐dependent manner.Meanwhile, rucaparib suppressed cell cycle progression in the s phase and promoted apoptosis in a dose‐dependent manner.Further, combination of inpp4b overexpression and rucaparib declined myc, cyclin e1 and cyclin d1 expressions, enhanced bad, bax, and cleaved‐caspase‐3 expressions, and blocked pi3k/akt signal pathway in sa os2 and u2os cells.Finally, combination of inpp4b overexpression and rucaparib inhibited tumor formation in vivo.The study demonstrated that inpp4b and rucaparib exhibited synergistic antitumor effect by regulating pi3k/akt pathway in os cells.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Triptolide inhibits the proliferation and migration of medulloblastoma Daoy cells by upregulation of microRNA-138

Medulloblastoma is a primitive neuroectodermal‐derived brain tumor and the most common malignant brain tumor in children.Triptolide (tpl) is the major active component extracted from tripterygium wilfordii hook f.This study aimed to explore the effects of tpl on medulloblastoma cell proliferation, migration, and apoptosis, as well as the underlying possible molecular mechanism.Viability, proliferation, and apoptosis of daoy cells were measured using cell counting kit‐8 assay, 5‐bromo‐2′‐deoxyuridine incorporation assay, and guava nexin assay, respectively.Cell migration was detected using two‐chamber transwell assay and wound healing assay.Quantitative reverse transcription polymerase chain reaction (q rt‐pcr) was performed to determine the relative expression of micro rna‐138 (mi r‐138) in daoy cells.Cell transfection was used to change the expression of mi r‐138 in cells.Western blot analysis was used to analyze the expression of key factors involved in cell apoptosis, cell migration, the phosphatidylinositol 3‐kinase (pi3k)/protein kinase 3 (akt) pathway, and the notch pathway in daoy cells.We found that tpl significantly inhibited the viability, proliferation, and migration of daoy cells but promoted daoy cell apoptosis.The expression levels of matrix metalloproteinases (mmp)‐2 and mmp‐9 after tpl treatment were decreased.The expression of mi r‐138 in daoy cells after tpl treatment was increased.Suppression of mi r‐138 obviously reversed the tpl‐induced daoy cell proliferation, migration inhibition, and cell apoptosis enhancement, as well as the inactivation of the pi3k/akt and notch pathways.Cyclin‐dependent kinase 6 (cdk6) was a direct target gene of mi r‐138, which might be involved in the antitumor effects of tpl on daoy cells.In conclusion, our study verified that tpl exerted anticancer effects on medulloblastoma cells possibly via upregulating mi r‐138 and inactivating the pi3k/akt and notch pathways.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Long non-coding RNA reprogramming (lncRNA-ROR) regulates cell apoptosis and autophagy in chondrocytes

Long non‐coding rna reprogramming (lnc rna‐ror) plays an important role in regulating various biologic processes, whereas the effect of lnc rna‐ror in osteoarthritis (oa) is little studied.This study aimed to explore lnc rna‐ror expression in articular cartilage and identify the functional mechanism of lnc rna‐ror in oa.Oa cartilage tissues were obtained from 15 oa patients, and 6 normal cartilage tissues were set as controls.Chondrocytes were isolated from the collected cartilage tissues.Lnc rna‐ror was knockdown in normal cells and overexpressed in oa cells.Cell viability was determined with cell counting kit‐8 assay, and apoptosis was measured using flow cytometric analysis.Moreover, proteins and m rnas involved in this study were also measured using western blotting and quantitative real‐time pcr (q pcr).Level of lnc rna‐ror was decreased in oa compared with normal chondrocytes, and overexpression of lnc rna‐ror dramatically promoted cell viability of oa chondrocytes.In addition, knockdown lnc rna‐ror inhibited apoptosis and promoted autophagy of normal chondrocytes.Moreover, lnc rna‐ror inhibited the expression of p53 in both m rna and protein levels.Furthermore, we revealed that lnc rna‐ror regulated apoptosis and autophagy of chondrocytes via hif1α and p53.The results indicated that lnc rna‐ror played a critical role in the pathogenesis of oa, suggesting that lnc rna‐ror could serve as a new potential therapeutic target for oa.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;