syedzayyan/paper_mill_benchmark huggingface dataset:
Down-regulated long non-coding RNA ANRIL restores the learning and memory abilities and rescues hippocampal pyramidal neurons from apoptosis in streptozotocin-induced diabetic rats via the NF-κB signaling pathway

Diabetes often causes learning and memory deficits, which leads to unfavorable behavioral performance.In this study, we investigated the effects of long non‐coding rna (lnc rna) anril on learning, memory abilities, and hippocampal neuronal apoptosis via the nf‐κb signaling pathway in streptozotocin (stz)‐induced diabetic rats.After successful establishment of diabetic rat models, the subjects were then assigned into the dm, dm + si‐anril, dm + si‐negative control (si‐nc) groups, as well as an additional normal group.Morris water maze test was employed to assess behavioral performance of rats, followed by the recording of body weight and blood glucose levels.Expressions of anril, nf‐κb signaling pathway‐related, and apoptosis‐related genes were examined by q rt‐pcr and western blotting.Rat hippocampus expression levels of cleaved‐caspase‐3 were determined by immunofluorescence.Cell apoptosis was examined by tunel assay.Versus to the normal group, revealed there to be activation of the nf‐κb signaling pathway, decreased weight, increased blood glucose, increased escape latency, reduced residence time, memory impairment, increased cleaved‐caspase‐3 expression, and increased apoptosis were detected in the dm and dm + si‐nc groups.The dm + si‐anril group exhibited inhibited nf‐κb signaling pathway, weight loss, decreased blood glucose, recovered memory, decreased cleaved‐caspase‐3 expression and reduced apoptosis compared to the dm group, with higher weight of rats, lower blood glucose levels, and stronger memory abilities in the dm + si‐anril group.Taken together, these findings indicate that silencing lnc rna anril promotes memory recovery and decreases hippocampal neurons apoptosis in diabetic rats through the inhibition of the nf‐κb signaling pathway.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-183 induces epithelial-mesenchymal transition and promotes endometrial cancer cell migration and invasion in by targeting CPEB1

The aim of this study is to evaluate the ability of micro rna‐183 (mi r‐183) to influence epithelial‐mesenchymal transition (emt) and cell proliferation, migration, invasion, and apoptosis in endometrial cancer (ec) by targeting cytoplasmic polyadenylation element binding protein 1(cpeb1).Ec tissues with matched nonmalignant tissues were collected from 208 ec patients.Ishikawa and rl95‐2 cells were selected for cell experiments in vitro and each kind of cells were grouped into blank, negative control (nc), mi r‐183 mimic, mi r‐183 inhibitor, cpeb1 overexpression, and mi r‐183 mimic + cpeb1 overexpression groups.Expressions of mi r‐183, cpeb1, e‐cadherin, and vimentin were determined by reverse transcription quantitative polymerase chain reaction (rt‐q pcr) and western blotting.Cell viability, colony formation ability, migration, invasion, and apoptosis were assessed by mtt assay, clone formation assay, scratch test, transwell assay, and flow cytometry.In vivo tumorigenesis of ishikawa cells was evaluated by tumor formation in nude mice.The mi r‐183 expression was higher, but the cpeb1 expression was lower in ec tissues than in adjacent nonmalignant tissues.Cpeb1 was confirmed as the target of mi r‐183 by dual‐luciferase reporter assay.The mi r‐183 mimic group had increased cell viability, colony formation ability, cell invasion and migration, tumor volume and weight in nude mice, but decreased cell apoptosis when compared with the blank group.The expression of e‐cadherin was down‐regulate, but expression of vimentin was up‐regulate in the mi r‐183 mimic group in comparison with the blank group.In terms of a comparison between the blank group and cpeb1 overexpression group, the cpeb1 overexpression group had suppressed cell viability, colony formation ability, cell invasion and migration, tumor volume and weight, but increased cell apoptosis.The expression of e‐cadherin was up‐regulated, but the expression of vimentin was down‐regulated in the cpeb1 overexpression group in comparison with the blank group.The mi r‐183 mimic + cpeb1 overexpression group had higher mi r‐183 expression than the blank group.These findings indicate that mi r‐183 induces emt, inhibits apoptosis, and promotes cell proliferation, migration, invasion, and in vivo tumorigenesis in ec by targeting cpeb1.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Silencing of COL1A2, COL6A3, and THBS2 inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the PI3k-Akt signaling pathway

This study explores the effect of col1a2, col6a3, and thbs2 gene silencing on proliferation, migration, invasion, and apoptosis of gastric cancer cells through the pi3k‐akt signaling pathway.The gastric cancer microarray expression data (gse19826, gse79973, and gse65801) was analyzed.Gastric cancer tissues and corresponding adjacent normal tissues were extracted from patients.Positive expression rate of pi3k, akt, and p‐akt was measured with immunohistochemistry.Two cell lines, bgc‐823 and sgc‐7901, were transfected and cells were grouped into blank, negative control, col1a2‐sh rna, col6a3‐sh rna, and thbs2‐sh rna groups.Expressions of col1a2, col6a3, and thbs2 in gastric cancer cells transfected with corresponding silencing sequences were evaluated by rt‐q pcr and western blot.Mtt assay, transwell, and cell scratch tests were conducted to evaluate cell proliferation, invasion, and migration capacity, respectively.Flow cytometry was used to evaluate cell cycle distribution and apoptosis.The positive expression of pi3k, akt, and p‐akt was higher in gastric cancer tissues compared with adjacent normal tissues, and the m rna expression of col1a2, col6a3, and thbs2 was increased in gastric cancer tissues.Akt, p‐akt, and pi3k expression drastically decreased in cells transfected with col1a2, col6a3, and thbs2 silencing sequences.Cells transfected with col1a2, col6a3, and thbs2 silencing sequences exhibited promoted apoptosis but inhibited proliferation, migration, and invasion.This study demonstrates that col1a2, col6a3, and thbs2 gene silencing inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the pi3k‐akt signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
MicroRNA-184 inhibits proliferation and promotes apoptosis of human colon cancer SW480 and HCT116 cells by downregulating C-MYC and BCL-2

This study aimed to investigate the effects of micro rna‐184 (mi r‐184) on the proliferation and apoptosis of human colon cancer cells through the regulation of c‐myc and bcl‐2.Human colon cancer tissues were selected as case group, and adjacent normal tissues were as control group.Human colon cancer sw480 and hct116 cells were allocated into blank, mi r‐184 mimic negative control (mimic‐nc), mi r‐184 inhibitor nc (inhibitor‐nc), mi r‐184 mimic, and mi r‐184 inhibitor groups.Flow cytometry, annexin v/pi and mtt assay were used to examine the cell cycle, apoptosis and viability.The expressions of c‐myc, bcl‐2 and mi r‐184 were detected via immunohistochemistry, western blotting and reverse transcription quantitative polymerase chain reaction (rt‐q pcr).C‐myc and bcl‐2 were direct targets to mi r‐184.The growth of colon cancer cells in the mi r‐184 mimic group was inhibited and exhibited an increase in apoptosis.Cell growth in the mi r‐184 mimic group was increased in addition to the inhibition of apoptosis.Compared with mi r‐184 mimic group, the expressions of c‐myc and bcl‐2 in mi r‐184 inhibitor group were increased.The expressions of c‐myc and bcl‐2 in colon cancer tissues exhibited high levels of expression, while mi r‐184 displayed relatively low levels in comparison to the adjacent normal tissues.An association was detected regarding the expressions of mi r‐184, c‐myc and bcl‐2 with the differentiation, invasion depth and lymph node metastasis.Mi r‐184 expression was negatively related to c‐myc and bcl‐2 expressions.Our study suggested that mi r‐184 could inhibit proliferation and promote apoptosis of colon cancer cells by down‐regulating expressions of c‐myc and bcl‐2.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Potential Role of Long Non-Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on Proliferation and Migration by Targeting miR-323

Medulloblastoma (mb) is a common primary tumor of the central nervous system diagnosed in pediatric patients.Survivors of mb are frequently accompanied by severe side effects, thus it is urgent to explore novel therapeutic target.First of all, the level of antisense non‐coding rna in the ink4 locus (anril) in normal cerebellum and daoy cells were evaluated.Then, the effect of anril on daoy cell proliferation, migration, and apoptosis were tested.Then, q rt‐pcr was performed to explore whether anril acted as a sponge of mi r‐323.The effects of mi r‐323 inhibition on anril silence‐induced alterations of cell proliferation, migration, and apoptosis were estimated.Predicted by target scan, the possible target gene of mi r‐323 was screened, followed by validation with luciferase assay.The abnormally expressed bri3 on cell proliferation, migration, apoptosis, and signaling pathways were all evaluated.Anril was up‐regulated in mb and its silence significantly lowered cell viability and migration but promoted cell apoptosis.Anril acted as a sponge of mi r‐323 and its silence functioned through up‐regulating mi r‐323.Bri3 and cdk6 were target genes of mi r‐323 and the effect of bri3 on daoy cells was the same as anril.Moreover, anril suppression could reduce phosphorylated levels of p38 mapk, erk and akt, and inhibit wnt signaling pathway through positively regulating bri3.Anril inhibition repressed cell proliferation and migration but promoted cell apoptosis through mi r‐323‐mediated regulation of bri3, which could activate p38 mapk, erk, and akt as well as wnt signaling pathway.J.Cell.Biochem.118: 4735–4744, 2017.© 2017 wiley periodicals, inc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Long noncoding RNA MT1JP inhibits proliferation, invasion, and migration while promoting apoptosis of glioma cells through the activation of PTEN/Akt signaling pathway

This study is carried out to elucidate the role of long noncoding rnas (lnc rnas) mt1jp in proliferation, invasion, migration, and apoptosis of glioma cells through the regulation of pten/akt signaling pathway.The expression of mt1jp in 80 normal brain tissues and 138 glioma tissues, as well as glioma cell lines, was detected by quantitative reverse‐transcription polymerase chain reaction.Besides, glioma cells with overexpression and low expression of mt1jp were constructed to confirm the role of mt1jp in proliferation, invasion, migration, and apoptosis of glioma cells and the growth of glioma cells in vivo through the regulation of pten/akt signaling pathway.Mt1jp expression was downregulated in glioma tissues and cells.The low expression of mt1jp was considered as an independent risk factor for predicting overall survival in gliomas.After transfection of mt1jp overexpression plasmid, glioma cells showed decreased proliferation, migration and invasion ability, increased apoptosis rate, and decreased the tumorigenic ability of nude mice.The trends were opposite in glioma cells transfected with mt1jp poor expression plasmid.Collectively, our study suggests that lnc rna mt1jp is responsible for inhibiting proliferation, invasion, and migration while promoting apoptosis of glioma cells through the activation of pten/akt signaling pathway.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
MicroRNA-150 contributes to ischemic stroke through its effect on cerebral cortical neuron survival and function by inhibiting ERK1/2 axis via Mal

Ischemic stroke, caused by the blockage of blood supply, is a major cause of death worldwide.For identifying potential candidates, we explored the effects micro rna‐150 (mi r‐150) has on ischemic stroke and its underlying mechanism by developing a stable middle cerebral artery occlusion (mcao) rat model.Gene expression microarray analysis was performed to screen differentially expressed genes associated with mcao.We evaluated the expression of mi r‐150 and mal and the status of erk1/2 axis in the brain tissues of mcao rats.Then the cerebral cortical neurons (ccns) were obtained and introduced with elevated or suppressed mi r‐150 or silenced mal to validate regulatory mechanisms for mi r‐150 governing mal in vitro.The relationship between mi r‐150 and mal was verified by dual luciferase reporter gene assay.Besides, cell growth and apoptosis of ccns were detected by means of mtt assay and flow cytometry analyses.We identified mal as a downregulated gene in mcao, based on the microarray data of gse16561.Mi r‐150 was over‐expressed and negatively targeted mal in the brain tissues obtained from mcao rats and their ccns.Increasing mi r‐150 blocked the erk1/2 axis, resulting in an inhibited cell growth of cnns but an enhanced apoptosis.Furthermore, mi r‐150 inhibition was observed to have effects on cnns as opposed to those inhibited by mi r‐150 promotion.The key findings of this study support the notion that mi r‐150 under‐expression‐mediated direct promotion of mal protects cnn functions through the activation of the erk1/2 axis, and underscore the concept that mi r‐150 may represent a novel pharmacological target for ischemic stroke intervention.

Journal: Journal of Cellular Physiology (2018)
Publication types: Research Article;
MicroRNA-21 contributes to high glucose–induced fibrosis in peritoneal mesothelial cells in rat models by activation of the Ras–MAPK signaling pathway via Sprouty-1

Peritoneal fibrosis remains to be one of the most severe causes of failure in continuous peritoneal dialysis.The current study cultured peritoneal mesothelial cells in high glucose to stimulate the environment of peritoneal fibrosis model in rats, and investigate whether micro rna‐21 (mi r‐21) targeting sprouty‐1 affects high glucose–induced fibrosis in peritoneal mesothelial cells via the rennin angiotensin system (ras)–mitogen‐activated protein kinase (mapk) signaling pathway, as well as potential mechanisms.Peritoneal tissues in fibrosis rats were collected to extract peritoneal mesothelial cells, which, after in vitro culture, were transfected with a series of mimic or inhibitor of mi r‐21, or the small interfering rna (si rna) against sprouty‐1.Reverse‐transcription quantitative polymerase chain reaction and western blot analyses were performed to determine the levels of related genes or proteins.Mtt assay and flow cytometry were conducted to observe the cell viability and cell apoptosis of peritoneal mesothelial cells.Dual‐luciferase reporter gene assay revealed that sprouty‐1 is the target gene of mi r‐21.Peritoneal fibrosis manifested with elevated mi r‐21, extracellular‐signal‐regulated kinase (erk), c‐jun nh2‐terminal protein kinase (jnk), ras and p38mapk but reduced sprouty‐1.Cells transfected with mi r‐21 mimic exhibited decreased sprouty‐1 expressions, but increased levels of erk, jnk, ras, and p38mapk.As for cellular process, mi r‐21 mimic or si rna against sprouty‐1 exposure reduced cell viability, which resulted in more cells arrested at the g1 stage, and induced apoptosis.In contrast, mi r‐21 inhibitor exposure was observed to have induced effects on peritoneal mesothelial cells.These key findings provide evidence that mi r‐21 inhibits sprouty‐1 to promote the progression of fibrosis in peritoneal mesothelial cells by activating the ras–mapk signaling pathway.

Journal: Journal of Cellular Physiology (2018)
Publication types: Research Article;
In vivo and in vitro effects of microRNA-221 on hepatocellular carcinoma development and progression through the JAK–STAT3 signaling pathway by targeting SOCS3

Hepatocellular carcinoma (hcc), as the third leading cancer‐caused deaths, prevails with high mortality, and affects more than half a million individuals per year worldwide.A former study revealed that micro rna‐221 (mi r‐221) was involved in cell proliferation of liver cancer and hcc development.The current study aims to evaluate whether mi r‐221 targeting socs3 affects hcc through jak–stat3 signaling pathway.A series of mi r‐221 mimic, mi r‐221 inhibitor, si rna against socs3 , and socs3 plasmids were introduced to smmc7721 cells with the highest mi r‐221 expression assessed.The expression of jak–stat3 signaling pathway–related genes and proteins was determined by western blot analysis.Cell apoptosis, viability, migration, and invasion were evaluated by means of flow cytometry, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5 diphenyl tetrazolium bromide, and transwell assays, respectively.Hcc xenograft in nude mice was performed to measure hcc tumor growth.Mi r‐221 was found to be highly expressed but socs3 was poorly expressed in hcc tissues.Mi r‐221 expression was correlated with lymph node metastasis (lnm) and tumor node metastasis (tnm) of hcc, and socs3 expression was correlated with lnm, differentiation and tnm of hcc.Socs3 is a target gene of mi r‐221.Mi r‐221 mimic or si‐socs3 exposure was found to induce cell viability, migration, and invasion, and reduce apoptosis.Mi r‐221 inhibitor was observed to have inhibitory effects on hcc cell proliferation, migration, and invasion.Moreover, the expression of jak–stat3 signaling pathway was suppressed by mi r‐221 inhibitor.Downregulated mi r‐221 expression could promote its target gene socs3 to inhibit the proliferation, invasion and migration of hcc cells by repressing jak–stat3 signaling pathway.

Journal: Journal of Cellular Physiology (2018)
Publication types: Research Article;
Effect of microRNA-186 on oxidative stress injury of neuron by targeting interleukin 2 through the janus kinase-signal transducer and activator of transcription pathway in a rat model of Alzheimer's disease

Recent studies have proposed that micro rnas (mi r) function as novel diagnostic and prognostic biomarkers and therapeutic targets in alzheimer’s disease (ad), a common disease among the elderly.In the current study, we aim to explore the effect of mi r‐186 on oxidative stress injury of neuron in rat models of ad with the involvement of the interleukin‐2 (il2) and the janus kinase/signal transducers and activators of transcription (jak–stat) pathways.Ad rat models were established, and dual‐luciferase reporter assay and online software were used to confirm the targeting relationship between mi r‐186 and il2.Immunohistochemistry was used evaluating the positive rate of il2.Afterward, to define the role of mi r‐186 in ad, mi r‐186, il2, and jak–stat related protein (jak2, stat3) expressions were quantified.Cell proliferation was measured by 3‐(4,5‐dimethylthiazol‐2‐yl)2,5‐diphenyl tetrazolium bromide, and cell apoptosis was detected by flow cytometry.We observed downregulated mi r‐186 and il2 and upregulated jak–stat signaling pathway related genes in ad.The overexpression of mi r‐186 was shown to significantly promote cell proliferation while suppressing cell apoptosis along with the expression of the il2 and jak–stat signaling pathway related protein.Collectively, the key findings obtained from the current study define the potential role of mi r‐186 as an inhibitor of ad development by downregulation of il2 through suppression of the jak–stat signaling pathway.

Journal: Journal of Cellular Physiology (2018)
Publication types: Research Article;
Downregulated expression of microRNA-329 inhibits apoptosis of nigral dopaminergic neurons by regulating CDKN2D expression via the FoxO3a signaling pathway in rats with Parkinson's disease

Parkinson's disease (pd) is a common neurodegenerative disorder due to the loss of dopaminergic neurons in the substantia nigra.This study focuses on the effect of micro rna‐329 (mi r‐329) on nigral dopaminergic neurons in a rat model of pd via the fox o3a signaling pathway by binding to cdkn2d.Brain tissues from the substantia nigra were taken from the rats in two groups.Tunel staining was used to observe tyrosine hydroxylase (th)‐positive neurons.Nigral dopaminergic neurons were randomized into the normal, blank, negative control (nc), mi r‐329 mimics, mi r‐329 inhibitors, small interfering (si rna)‐cdkn2d, and mi r‐329 inhibitors + si rna‐cdkn2d groups.Expressions of mi r‐329, cdkn2d, fox o3a, akt, caspase‐3 and bcl‐2 were determined using rt‐q pcr and western blotting.Apoptosis rate of nigral dopaminergic neurons in 7 groups was determined by flow cytometry.Compared with the blank and nc groups, the mi r‐329 mimics group showed increased mi r‐329 and caspase‐3 expressions as well as decreased expressions of cdkn2d, fox o3a, akt, and bcl‐2, the si rna‐cdkn2d group indicated enhanced expressions of caspase‐3 and declined expressions of cdkn2d, fox o3a, akt, and bcl‐2, and the mi r‐329 inhibitors group revealed decreased mi r‐329 and caspase‐3 expressions and increased expressions of cdkn2d, fox o3a, akt, and bcl‐2.The apoptosis rate of nigral dopaminergic neurons was significantly increased in the mi r‐329 mimics and si rna‐cdkn2d groups, but was decreased in the mi r‐329 inhibitors group.Our data suggested that downregulated mi r‐329 could inhibit apoptosis of nigral dopaminergic neurons in a rat model of pd by upregulating the expression of cdkn2d via the activation of the fox o3a signaling pathway.

Journal: Journal of Cellular Physiology (2018)
Publication types: Research Article;
Effects of RNA interference-mediated silencing of toll-like receptor 4 gene on proliferation and apoptosis of human breast cancer MCF-7 and MDA-MB-231 cells: An in vitro study

Breast cancer is known as the most prevalent cancer in women worldwide, and has an undeniable negative impact on public health, both physically, and mentally.This study aims to investigate the effects of toll‐like receptor 4 (tlr4) gene silencing on proliferation and apoptosis of human breast cancer cells to explore for a new theoretical basis for its treatment.Tlr4 small interference rna (si rna) fragment recombinant plasmids were constructed, including tlr4 si rna‐1, tlr4 si rna‐2, and tlr4 si rna‐3.Human breast cancer mcf‐7 and mda‐mb‐231 cells were assigned into blank, negative control (nc), tlr4 si rna‐1, tlr4 si rna‐2, and tlr4 si rna‐3 groups.Mcf‐7 and mda‐mb‐231 cell growth was detected by mtt assay.Apoptosis and cell cycle were determined by flow cytometry.Reverse transcription quantitative polymerase chain reaction (rt‐q pcr) and western blot analysis were conducted to determine the expression of tlr4, cdk4, cyclin d1, livin, bcl‐2, p53, c‐flip, and caspase‐3.In comparison with the nc and blank groups, the tlr4 si rna‐1, tlr4 si rna‐2, and tlr4 si rna‐3 groups showed decreased the expression of tlr4, inhibited proliferation of mcf‐7 and mda‐mb‐231 cells and promoted mcf‐7 and mda‐mb‐231 cell apoptosis, and the cells were blocked in g1 phase.In comparison with the nc and blank groups, in the tlr4 si rna‐1, tlr4 si rna‐2, and tlr4 si rna‐3 groups, si rna‐tlr4 significantly increased expression of p53 and caspase‐3 in mcf‐7 and mda‐mb‐231 cells, while it decreased the expressions of cdk4, cyclin d1, livin, bal‐2, and c‐flip.The study demonstrates that tlr4 gene silencing inhibits proliferation and induces apoptosis of mcf‐7 and mda‐mb‐231 cells.

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