syedzayyan/paper_mill_benchmark huggingface dataset:
Microrna-139-5p inhibits epithelial-mesenchymal transition and fibrosis in post-menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway

The study explores whether mi r‐139‐5p targeting lpar4 affects epithelial‐mesenchymal transition (emt) and fibrosis in post‐menopausal women with interstitial cystitis (ic) via the pi3k/akt signaling pathway.Bladder tissues of ic and normal bladder tissues were collected.The pathology of bladder tissues was observed by he, masson and picrosirius red staining.Lpar4 positive expression rate were determined by ihc.Elisa was performed to detect the levels of il‐6, il‐8, il‐10, and tnf‐α.Rat ic models were randomized into seven different groups.Mi r‐139‐5p, lpar1, lpar2, lpar3, lpar4, lpar5, p13k, akt, e‐cadherin, n‐cadherin, vimentin, tgf‐β1, and ctgf expression were determined by rt‐q pcr and western blotting.Dual luciferase reporter gene assay verified that lpar4 is a target gene of mi r‐139‐5p.Fibrosis was a pathological manifestation of ic.The ic group showed higher lpar4, pi3k, akt, p‐pi3k, p‐akt, n‐cadherin, vimentin, tgf‐β1, and ctgf expression but lower mi r‐139‐5p and e‐cadherin expression than the normal group.The levels of il‐6, il‐8, il‐10, and tnf‐α expression decreased while hb‐egf increased in the ic group in comparison of the normal group.Compared with the blank and nc groups, e‐cadherin expression was increased in the mi r‐139‐5p mimic and si rna‐lpar4 groups, while lpar4, pi3k, akt, p‐p13k, p‐akt, n‐cadherin, vimentin, tgf‐β1, and ctgf expression were decreased.An opposite trend was found in the mi r‐139‐5p inhibitor group.The mi r‐139‐5p decreased in the mi r‐139‐5p inhibitor + si rna‐lpar4 and mi r‐139‐5p inhibitor + wortmannin groups.Conclusively, mi r‐139‐5p targeting lpar4 inhibits emt and fibrosis in post‐menopausal ic women through the pi3k/akt signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of long non-coding RNA HOST2 on cell migration and invasion by regulating MicroRNA let-7b in breast cancer

The study intends to investigate the effects of long non‐coding rna host2 (lnc rna host2) on cell migration and invasion by regulating micro rna let‐7b (let‐7b) in breast cancer.Breast cancer and adjacent normal tissues were collected from 98 patients with breast cancer.Breast cancer mcf‐7 cells were divided into the blank, negative control (nc), pc dna3‐mock, si host2, let‐7b inhibitor, pc dna3‐host2, let‐7b mimic, pc dna3‐host2 + let‐7b mimic, and si host2 + let‐7b inhibitor groups.Rt‐q pcr was used to detect the m rna expressions of host2, let‐7b, and c‐myc.Western blotting was conducted to measure the c‐myc expression.Scratch test and transwell assay were applied to detect the cell motility, migration, and invasion.Xenograft tumor in nude mice was performed to evaluate the effect of different transfection on the tumor growth.Compared with adjacent normal tissues, host2 expression was higher but let‐7b expression lower in breast cancer tissues.Host2 expression in breast cancer cells was remarkably increased compared with that in the normal breast epithelial mcf‐10a cells.In mcf‐7 cells, in comparison with the blank and nc groups, expressions of host2 and c‐myc were reduced, but let‐7b expression was remarkably elevated in the si host2 and let‐7b mimic groups; the let‐7b inhibitor group exhibited higher expressions of host2 and c‐myc but lower let‐7b expression.Overexpression of host2 could promote cell motility, migration and invasion, thus enhancing the growth of breast cancer tumor.By inhibiting host2, opposite trends were found.Lnc rna host2 promotes cell migration and invasion by inhibiting let‐7b in breast cancer patients.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of microRNA-330 on vulnerable atherosclerotic plaques formation and vascular endothelial cell proliferation through the WNT signaling pathway in acute coronary syndrome

This study is designed to investigate the effects of micro rna (mi r)‐330 on atherosclerotic plaques formation and vascular endothelial (ve) cell proliferation by targeting mapk8 through the wnt signaling pathway in rats with acute coronary syndrome (acs).Expression of hemodynamic variables were tested.Rats were allocated into control, blank, negative control (nc), mi r‐330 mimic, mi r‐330 inhibitor, ddk‐1, mi r‐330 inhibitor + ddk‐1 groups.Elisa was used to evaluate the expression of tc, tg, ldl‐c, hs‐crp, il‐6, il‐10, tnf‐α, and saa.Immunohistochemistry, reverse transcription quantitative polymerase chain reaction and western blotting were used for expression of vegf, mapk8, wnt1, β‐catenin, gsk‐3β, p‐gsk‐3β, cyclin d1, mmp‐9, il‐6, and il‐8.Mtt assay and flow cytometry for cell proliferation and apoptosis.Compared with the control group, other groups had lower levels of sbp, dbp, mbp, lvsp, and mi r‐330, higher levels of hr, lvedp, tc, tg, ldc‐c, hs‐crp, il‐6, il‐10, tnf‐α, saa, higher positive protein expression rates of mapk8, vegf, and mmp‐9, elevated wnt1, β‐catenin, gsk‐3β and cyclin d1, and reduced cell proliferation.Mapk8‐3'‐utr was targeted by mi r‐330.Compared with the blank group, the mi r‐330 mimic and ddk‐1 groups had higher levels of sbp, dbp, mbp, lvsp, lower levels of hr, lvedp, tc, tg, ldc‐c, hs‐crp, il‐6, tnf‐α, saa, elevated il‐10, decreased positive protein expression rates of mapk8 and vegf, raised cell proliferation and reduced cell apoptosis rates.We conclude that overexpressed mi r‐330 suppresses atherosclerotic plaques formation while promotes ve cell proliferation by targeting mapk8 through the wnt signaling pathway in acs rats.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effect of the Wnt/β-catenin signaling pathway on apoptosis, migration, and invasion of transplanted hepatocellular carcinoma cells after transcatheter arterial chemoembolization in rats

This study aims to investigate the influence of the wnt/β‐catenin signaling pathway on apoptosis, migration, and invasion of transplanted hepatocellular carcinoma (hcc) cells after transcatheter arterial chemoembolization (tace) in rat models.A total of 80 rats were grouped into sham, tace, wnt‐c59, and tace + wnt‐c59 groups ( n = 20).Ten days after model establishment, 10 rats in each group were executed to perform pathological examination and follow‐up experiment, and the remaining 10 rats in each group were reared to observe the survival condition.Rt‐q pcr and western blotting were applied to determine the expressions of wnt1, β‐catenin, cyclin d1, c‐met, vimentin, e‐cadherin, and vascular endothelial growth factor (vegf).Elisa was performed to measure the serum alpha‐fetoprotein (afp) content of rats.Flow cytometry was used to evaluate cell apoptosis rate and transwell assay to examine cell migration and invasion.Compared with the tace group, the wnt‐c59 and tace + wnt‐c59 groups showed increased apoptosis and survival time (the tace + wnt‐c59 group &gt; the wnt‐c59 group).Compared with the sham group, the tace + wnt‐c59 groups showed decreased cancer tissue weight and expressions of wnt1, β‐catenin, cyclin d1, vimentin, c‐met, and vegf, but increased e‐cadherin expression.Compared with the tace group, the wnt‐c59 and tace + wnt‐c59 groups showed decreased afp level, migration, and invasion (the tace + wnt‐c59 group &lt; the wnt‐c59 group).These findings indicate inhibition of the wnt/β‐catenin signaling pathway improves therapeutic effect on tace via suppressing migration, invasion, and promoting apoptosis of transplanted hcc cells in rats.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Effects of S100A12 gene silencing on serum levels of anti-inflammatory/pro-inflammatory cytokines in septic rats through the ERK signaling pathway

We explored the effect of s100a12 gene on serum levels of anti‐inflammatory/pro‐inflammatory cytokines in septic rats by activating the extracellular signal‐regulated kinase (erk) signaling pathway.A total of 180 specific pathogen‐free (spf) rats were purchased to establish cecal ligation and puncture (clp) model.Rats were assigned into the sham, model, empty vector, s100a12 si rna, epidermal growth factor (egf), and s100a12 si rna + egf groups.The expressions of s100a12, erk‐1, erk‐2, c pla2, and nf‐κb in liver tissues of rats among six groups were detected by rt‐q pcr and western blotting.Elisa was used to determine serum levels of il‐1β, il‐10, tnf‐α, procalcitonin (pct), and c‐reactive protein (crp).Pearson correlation analysis was conducted to measure correlations.Cell apoptosis of rats among six groups was detected by tunel staining.The expressions of s100a12, erk‐1, erk‐2, c pla2, and nf‐κb decreased in the s100a12 si rna group while increased in the egf group compared with the model group.S100a12 m rna expression was positively correlated with m rna expressions of related genes in the erk signaling pathway (erk‐1, erk‐2, c pla2, and nf‐κb) in the model and empty vector groups.Expressions of il‐1β, il‐6, tnf‐α, pct, and crp in the egf group were higher than those in the model group, but were lower than those in the s100a12 si rna group.Compared with the model group, cell apoptosis decreased in the s100a12 si rna group but that increased in the egf group.We demonstrates that s100a12 gene silencing decreases serum levels of anti‐inflammatory/pro‐inflammatory cytokines in septic rats by inhibiting the erk signaling pathway.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Effects of microrna-93 on mouse cardiac microvascular endothelial cells injury and inflammatory response by mediating SPP1 through the NF-ΚB pathway

Background this study aims to investigate the regulative role of micro rna‐93 (mi r‐93) in mouse cardiac microvascular endothelial cells (cmecs) injury and inflammatory response by negatively targeting spp1 gene via the nf‐κb signaling pathway.Methods healthy balb/c mice were recruited to establish a mouse model with myocarditis using the cvb3 virus.Mice were grouped into normal, blank, negative control (nc), mi r‐93 inhibitor, mi r‐93 mimic, spp1 short hairpin rna (sh rna), and mi r‐93 mimic+spp1 sh rna groups.Reverse transcription quantitative polymerase chain reaction and western blot analysis were applied to determine the expressions of mi r‐93, spp1, vegfa, p50, p65, bax, and bcl‐2.Mtt assay was conducted to evaluate cell viability, annexin v‐fluorescein isothiocyanate/propidium iodide double staining was conducted to examine cell apoptosis, enzyme‐linked immunosorbent assay was conducted to measure secretion of inflammatory factors, and chemical colorimetry was conducted to determine no secretion.Results spp1 was a target gene of mi r‐93.Compared with the normal group, other six groups showed increased expressions of spp1, p50, p65, vegfa, and bax, as well as cell apoptosis rate and secretion of cell inflammatory factors, and decreased expression of bcl‐2, cell viability, and no secretion.Compared with the blank group, the mi r‐93 inhibitor group showed elevated expressions of spp1, p50, p65, vegfa, and bax, as well as cell apoptosis rate and secretion of cell inflammatory factors, and reduced bcl‐2, cell viability, and no secretion.While the mi r‐93 mimic and spp1 sh rna groups displayed opposite results.Conclusion taking our results together, we conclude that upregulation of mi r‐93 reduces cmecs injury and inflammatory response by negatively targeting spp1 via inactivating the nf‐κb signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
MicroRNA-106b overexpression alleviates inflammation injury of cardiac endothelial cells by targeting BLNK via the NF-κB signaling pathway

We aim to investigate whether micro rna‐106b (mi r‐106b) affects the inflammation injury of cardiac endothelial cells (ecs) by targeting b‐cell linker (blnk) via the nf‐κb signaling pathway.Human cardiac microvascular endothelial cells (hcmecs) were assigned into the control, hypoxia/reoxygenation (h/r), negative control (nc), pyrrolidine dithiocarbamate (pdtc), mi r‐106b mimic, mi r‐106b inhibitor, and si‐blnk, and mi r‐106b inhibitor+si‐blnk groups.Quantitative real‐time polymerase chain reaction (q rt‐pcr) and western blotting were conducted for mi r‐106b expression and expressions of blnk, interleukin (il)‐6, il‐1β, tumor necrosis factor (tnf)‐α, nf‐κb, p iκbα, btk, and plc‐γ2.Enzyme‐linked immunosorbent assay was applied for levels of il‐6, il‐10, and tnf‐α; cell counting kit‐8 assay for cell proliferation; and flow cytometry for cell cycle and ensuing apoptosis.In‐vitro tube formation assay was performed for tube formation ability.Dual‐luciferase reporter assay revealed that blnk was verified as the target gene of mi r‐106b.Compared with the h/r and nc groups, the pdtc, mi r‐106b mimic, and si‐blnk groups had declined expressions of il‐6, il‐1β, tnf‐α, btk, plc‐γ2, nf‐κb p105/p50, and p iκbα as well as levels of l‐6 and tnf‐α, but contrarily elevated levels of nf‐κb p105/p50 and il‐10.The pdtc, mi r‐106b mimic, and si‐blnk groups had less cell number in g 0 /g 1 phase but higher cell count in both s and g 2 phases, decreased cell apoptosis but increased proliferation and tube formation ability, while opposite trends were observed in the mi r‐106b inhibitor group.Our findings indicated that the overexpression of mi r‐106b alleviated the inflammation injury of cardiac ecs by targeting blnk via the nf‐κb signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of microRNA-24 targeting C-myc on apoptosis, proliferation, and cytokine expressions in chondrocytes of rats with osteoarthritis via MAPK signaling pathway

To investigate whether micro rna‐24 (mi r‐24) targeting c‐myc affects chondrocytes of rats with osteoarthritis (oa) via the mapk signaling pathway.Thirty rats were assigned as a sham group and an oa group (established as oa rat models by cutting the anterior cruciate ligaments and removing 1/3 medial meniscus).Tunel staining and immunohistochemistry were conducted for cell apoptosis index (ai) and positive expression rate of c‐myc protein.Enzyme‐linked immuno sorbent assay (elisa) was carried out for serum level of il‐1β and tnf‐α.Primary chondrocytes were assigned into the blank, negative control (nc), mi r‐24 mimics, mi r‐24 inhibitors, si rna‐ c‐myc , and mi r‐24 inhibitors+si rna‐ c‐myc groups.The expressions of mi r‐24, c‐myc, p38, erk, jnk, il‐1β, and tnf‐α in tissues and cells were detected using reverse transcription quantitative real‐time polymerase chain reaction (rt‐q pcr) and western blotting.Cck8 assay and flow cytometry were performed for cell proliferation and apoptosis.The oa group showed higher il‐1β, tnf‐α, ai, and c‐myc than the sham group.C‐myc is a target gene of mi r‐24.Compared with the blank group, the mi r‐24 mimics and si rna‐c‐myc groups showed reduced expression of c‐myc, il‐1β, tnf‐α, p38, p‐p38, erk, p‐erk, jnk, and p‐jnk, apoptosis rate yet increased cell proliferation; however, the mi r‐24 inhibitors group exhibited an opposite trend.The mi r‐24 inhibitors+si rna‐ c‐myc group presented a same tendency compared to the si rna‐ c‐myc group.Upregulated mi r‐24 downregulates c‐myc could suppress apoptosis and promote proliferation of chondrocytes to prevent the occurrence and subsequent progression of oa via inactivating the mapk signaling pathway.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-29b-3p prevents Schistosoma japonicum-induced liver fibrosis by targeting COL1A1 and COL3A1

Schistosomiasis is one of the world's major public health problems in terms of morbidity and mortality, causing granulomatous inflammation and cumulative fibrosis.This study explored in vivo and vitro effects of mi r‐29b‐3p in granulomatous liver fibrosis by targeting col1a1 and col3a1 in schistosoma japonicum infection.Thirty male balb/c mice were assigned to normal control and model (percutaneous infection of cercariae of s.Japonicum ) groups.Nih‐3t3 mouse embryonic fibroblasts were designated into blank, nc, mi r‐29b‐3p mimic, tgf‐β1, tgf‐β1 + nc, and tgf‐β1 + mi r‐29b‐3p mimic groups.He and masson staining were employed to observe the pathological changes and collagenous fibrosis.The expression of α ‐ sma, col1a1, col3a1, timp‐1 was determined by immunohistochemistry.The rt‐q pcr, western blotting and immunofluorescence staining were conducted to determine expression of mi r‐29b‐3p, col1a1, and col3a1.Cck‐8 assay and flow cytometry were performed to evaluate viability and apoptosis.The relative expression of mi r‐29b‐3p decreased in the model group.The model group showed marked fibrosis in liver tissues.The expression of α ‐ sma, col1a1, col3a1, timp‐1 was higher in the model group than that in the normal control group.Dual luciferase reporter gene assay revealed that mi r‐29b‐3p directly targeted col1a1 and col3a1.Compared with the blank, nc, tgf‐β1 and tgf‐β1 + nc groups, the mi r‐29b‐3p mimic group exhibited up‐regulated expression of mi r‐29b‐3p and mmp‐9 but down‐regulated expression of timp‐1, hsp47, α‐sma, col1a1, and col3a1; while lower cell viability but higher apoptosis rate showed.It indicated that mi r‐29b‐3p prevents s.Japonicum ‐induced liver fibrosis by inhibiting col1a1 and col3a1.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Effect of microRNA-128 on cisplatin resistance of glioma SHG-44 cells by targeting JAG1

This current study intends to investigate the effect of micro rna‐128 (mi r‐128) on cisplatin (ddp) resistance in glioma shg‐44 cells.Shg‐44/ddp cells were transfected with mi r‐128 antisense oligonucleotide (aso) and assigned into blank, resistance, nc, anti‐mi r‐128, mi r‐128 mimic, si‐jag1, and anti‐mi r‐128 + si‐jag1 groups.Q rt‐pcr and western blotting were employed for determining expression of mi r‐128, jag1, bax and bcl‐2.Mtt assay, giemsa staining, and flow cytometry were applied to detect ddp resistance, cellular morphology, and cell cycle, respectively.Jag1 is targeted and negatively regulated by mi r‐128.In in vitro experiments, compared with the blank group, the rest groups exhibited declined mi r‐28 and bax expression, lowered cell inhibition rate and apoptosis rate, but elevated jag1 and bcl‐2 expression with cells arrested in the s phase.Compared with the resistance group, the anti‐mi r‐128 group showed decreased bax expression along with a lowered cell inhibition rate and apoptosis rate, but increased jag1 and bcl‐2 expression with reduced cells arrested in the s phase; while the mi r‐128 mimic group showed an opposite trend; the si‐jag1 group showed decreased bcl‐2 expression and reduced cells in the s phase.In in vivo experiments, compared with the resistance group, the tumor growth rate, tumor volume, and weight as well as jag1 expression accelerated in the anti‐mi r‐128 group; whereas the mi r‐128 mimic and si‐jag1 groups exhibited an opposite trend.Our findings demonstrated that mi r‐128 aso transfection might down‐regulate the expression of mi r‐128 in shg‐44/ddp and up‐regulate the ddp resistance in shg‐44/ddp cells, providing a potential treatment target for glioma.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
MicroRNA-381-induced down-regulation of CXCR4 promotes the proliferation of renal tubular epithelial cells in rat models of renal ischemia reperfusion injury

This study aims to explore whether micro rna‐381 (mi r‐381) mediating cxcr4 affects the renal tubular epithelial cells (rtec) of renal ischemia reperfusion (i/r) injury.Forty‐eight rats were assigned into the i/r ( n = 24, successfully established as i/r model) and sham ( n = 24) groups.After collecting kidney tissues, immunohistochemistry, and microvascular density (mvd) counting were conducted for cxcr4 positive expression and mvd numbers.Rtecs were assigned into the sham, blank, negative control (nc), mi r‐381 mimics, mi r‐381 inhibitor, si‐ cxcr4 , and mi r‐381 inhibitor + si‐ cxcr4 groups.Rt‐q pcr and western blotting were performed for relative expressions in tissues and cells.Cell proliferation and apoptosis were measured by mtt assay and flow cytometry.Results showed that compared with the sham group, positive expression of cxcr4 and mvd number were higher in the i/r group, which exhibited decreased mi r‐381 and increased expression of cxcr4 , stromal cell‐derived factor‐1 (sdf1), vascular endothelial growth factor (vegf), hypoxia‐inducible factor 1 (hif‐1α) and tie‐2.Dual luciferase reporter gene assay verified that cxcr4 is a target gene of mi r‐381.Mi r‐381 expression was lower in the mi r‐381 inhibitor + si‐ cxcr4 and mi r‐381 inhibitor groups and higher in the mi r‐381 mimics group than the blank and nc groups.Compared with the blank and nc groups, the mi r‐381 mimics and si‐ cxcr4 groups exhibited higher cell proliferation but lower cell apoptosis and expression of cxcr4 , sdf1, vegf, hif‐1α, and tie‐2, whereas the mi r‐381 inhibitor group exhibited the opposite trend.In conclusion, mi r‐381 may promote rtec proliferation in rats with renal i/r injury by down‐regulating cxcr4 .

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-21 antisense oligonucleotide improves the sensitivity of A375 human melanoma cell to Cisplatin: An in vitro study

This study explored cisplatin resistance effect of micro rna‐21 (mi r‐21) antisense oligonucleotide (as‐odn) in human melanoma a375 cell.As‐odn was transfected in melanoma a375 cells and cisplatin‐resistant cell line a375/cddp, and divided into the as‐odn, nonsense oligonucleotide (ns‐odn) and normal groups.Cell ultrastructure changes were observed through transmission electron microscope.Mi r‐21 as‐odn could be tested cell growth effect in different time periods by trypan blue exclusion.Mi r‐21 m rna expression change was detected by quantitative fluorescence pcr.Cell apoptosis, cycle distribution and mi r‐21 as‐odn effect on proliferation and cisplatin sensitivity were tested by flow cytometry, mtt assay, tunel, and clonogenic assay.Cell apoptosis was observed after transfection 24 h with the as‐odn group, while the ns‐odn and normal group cells had no apoptotic symptoms; compared with the normal group, the as‐odn group began to show obvious cell growth inhibition effect after transfection 24 h lasting 72 h (all p &lt; 0.05), but the ns‐odn group had no significant difference ( p &gt; 0.05).Mi r‐21 m rna expression in the as‐odn group was obviously decreased with rising apoptosis rate (all p &lt; 0.05) and there was no significant difference in the ns‐odn group ( p &gt; 0.05).Mi r‐21 as‐odn could remarkably increase a375 cell and a375/cddp cell sensitivity to cisplatin ( p &lt; 0.05), while a375 cell sensitivity to cisplatin between the ns‐odn group and the normal group had no difference.Mi r‐21 as‐odn decreased ic 50 and increased cisplatin sensitivity for a375 cells and a375/cddp cells, which would be a new target of melanoma treatment.

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