syedzayyan/paper_mill_benchmark huggingface dataset:
LncRNA LINC00880 promotes cell proliferation, migration, and invasion while inhibiting apoptosis by targeting CACNG5 through the MAPK signaling pathway in spinal cord ependymoma

The present study was to investigate the effect of lnc rna linc00880 targeting cacng5 on cell proliferation, migration, invasion, and apoptosis in spinal cord ependymoma (sce) through the mapk signaling pathway.Geo database was used to download gene expression data related with sce (gse50161 and gse66354) and annotation file.Lnc rna with differential expression was predicted by multi experiment matrix website (mem).The target gene was analyzed by kegg pathway enrichment analysis.Sce tissues and adjacent tissues were collected.The positive expression of cacng5 protein was tested by immunohistochemistry.Expression of linc00880, cacng5, and mapk signaling pathway‐related proteins was measured with q rt‐pcr and western blotting.Cell proliferation, migration, invasion, cycle, and apoptosis were detected using mtt, transwell assay, scratch test, and flow cytometry.Sce tissues showed increased linc00880 expression.Cacng5 was a target gene of linc00880 and correlated with mapk signaling pathway.Compared with adjacent tissues, sce tissues showed lower positive expression of cacng5.Compared with the blank group, linc00880 expression was higher in the linc00880 vector and linc00880 vector + cacng5 vector groups, and lower in the si‐linc00880 and si‐linc00880 + si‐cacng5 groups; in the linc00880 vector and si‐cacng5 groups, expression of survivin, p38mapk, erk1/2, jnk1/2/3 increased and cacng5 and bax expression reduced, the proliferation, invasion and migration of tumor cells increased, and apoptosis rate decreased.Opposite results were found in the si‐linc00880 and cacng5 vector groups.The findings indicate that lnc rna linc00880 targeting cacng5 inhibits cell apoptosis and promotes proliferation, migration, and invasion in sce through the mapk signaling pathway.

Journal: Journal of Cellular Physiology (2017)
Publication types: Research Article;
Protective effects of Progranulin against focal cerebral ischemia-reperfusion injury in rats by suppressing endoplasmic reticulum stress and NF-κB activation in reactive astrocytes

The aim of this study is to explore the effect progranulin (pgrn) has on endoplasmic reticulum (er) stress and the nf‐κb activation in reactive astrocytes found in rat models with focal cerebral ischemia‐reperfusion (i/r) injury.Sprague‐dawley (sd) rats were grouped into the sham, i/r, pgrn‐high dose, pgrn‐low dose, and negative control (nc) groups.Ttc staining was applied in order to detect the cerebral infarction volume, a tunel assay to detect the apoptosis rate of neurons, an elisa to measure mda, sod, i nos, ldh, tnf‐α, il‐1β, il‐6, and il‐10 levels, and both rt‐q pcr and western blotting methods in order to detect pgrn, gfap, grp78, chop, and nf‐κb p65 expressions.The astrocytes (ast) cells were then assigned into the normal, i/r, negative control (nc), pgrn‐high dose, and pgrn‐low dose groups.After completing the transfection process, the proliferative capacity of ast cells was detected by use of the cck‐8 assay.Both the in vivo and in vitro results, in comparison with the i/r and the nc groups, the pgrn‐high dose and pgrn‐low dose groups both presented a decrease in cerebral infarction volume, apoptosis rate of neurons, mda, ldh, i nos, tnf‐α, il‐1β, il‐6 levels, and gfap, grp78, chop, nf‐κb p65 expressions, and an increase in sod, il‐10, and pgrn levels as well as cell proliferation depending on dosage.Based on our results, we came to the confirmation that pgrn can reduce neuronal apoptosis by mitigating er stress in the reactive astrocytes as well as downregulating the inflammatory levels by suppressing the nf‐κb signaling pathway.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-497 accelerates apoptosis while inhibiting proliferation, migration, and invasion through negative regulation of the MAPK/ERK signaling pathway via RAF-1

The aim of this study is to explore the various modes of action mi r‐497 has on human cervical cancer (cc) cell behavior.We also speculate that mi r‐497 achieves its anti‐tumor role by governing raf‐1 via mapk/erk signaling pathway.Cc tissues with corresponding adjacent normal tissues were collected from 168 cc patients.Raf‐1 ‐ positive cells were identified by means of immunohistochemistry in tissues.A series of inhibitors, mimics and si rna against raf‐1 were introduced to validate regulatory mechanisms for mi r‐497 and raf‐1.Quantitative real‐time polymerase chain reaction (q rt‐pcr) and western blot assay were employed for evaluating alternations of mi r‐497, raf‐1, and mapk/erk signaling pathway.He la cell proliferation, invasion, migration, cycle progression, and apoptosis were assessed by means of cck‐8, wound‐healing, transwell invasion assays, and flow cytometry, respectively.The target prediction program and luciferase activity determination were used to identify mi r‐497 targeting raf‐1.We determined reduced mi r‐497 expression and elevated expression of raf‐1 in cc tissues as opposed to adjacent tissues.Transfection of mi r‐497 mimics and si rna‐raf‐1 both decreased levels of mek1, erk1, and p38 phosphorylation in he la cells, inhibited cell proliferation, migration and invasion, induced more cells arrested in the g0/g1 phase, and promoted cell apoptosis; while mi r‐497 inhibitors led to opposite results.These findings indicate mi r‐497 as a tumor suppressor results from negative regulation of the mapk/erk signaling pathway via raf‐1 in cc.

Journal: Journal of Cellular Physiology (2017)
Publication types: Research Article;
MicroRNA-539 promotes osteoblast proliferation and differentiation and osteoclast apoptosis through the AXNA-dependent Wnt signaling pathway in osteoporotic rats

This study aims to explore the effects of mi r‐539 on osteoblast proliferation and differentiation and osteoclast apoptosis in a rat model of osteoporosis, and its mechanism involving the regulation of the axin1‐mediated wingless‐int (wnt) signaling pathway.A rat model of osteoporosis was successfully established by ovariectomy.With osteoblasts and osteoclasts of rats not receiving ovariectomy in the sham group as control, those of osteoporotic rats were treated with mi r‐539 inhibitor, mi r‐539 mimic, and axin1 sh rna.The expression of mi r‐53, axin1, the wnt pathway related‐genes, apoptosis related‐genes, and osteogenic markers were measured by rt‐q pcr and western blot analysis, respectively.Alkaline phosphatase (alp) activity in osteoblast and tartrate‐resistant acid phosphatase (trap) activity in osteoclasts were determined after cell transfection.Osteoblast and osteoclast viability was assayed by cck‐8 assay.Cell cycle and apoptosis of osteoblasts and osteoclasts were detected by flow cytometry.Lastly, alizarin red s staining was used to detect mineralized nodules of osteoblasts.Firstly, we determined that mi r‐539 was down‐regulated in osteoblast and osteoclast of osteoporotic rats and axin1 was negatively regulated by mi r‐539.Additionally, overexpression of mi r‐539 increased the expressions of β‐catenin, lef1, c‐myc, cyclin d1, runx2, bgp, bmp‐2 in osteoblast as well as β‐catenin, rho a, caspase‐3, and bcl‐2 in osteoclasts.Finally, overexpression of mi r‐539 elevated alp activity, proliferation, and mineralized nodules in osteoblast and osteoclast apoptosis, with reduced trap activity in osteoclasts.Our results demonstrate that mi r‐539 promotes osteoblast proliferation and differentiation as well as osteoclast apoptosis through the axin1‐dependent wnt signaling pathway in osteoporotic rats.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
The anti-inflammatory effect of microRNA-383-3p interacting with IL1R2 against homocysteine-induced endothelial injury in rat coronary arteries

Micro rnas (mi rs) are widely reported to be novel biomarkers involved in the process of coronary atherosclerosis (cas).Hence, this study aims to explore the function of mi r‐383‐3p targeting il1r2 on inflammatory injury of coronary artery endothelial cells (caecs) in cas.The underlying regulatory mechanisms of mi r‐383‐3p were analyzed in concert with the treatment of mi r‐383‐3p mimics, mi r‐383‐3p inhibitors, and the combination of mi r‐383‐3p inhibitors and si rna against il1r2 in homocysteine (hcy)‐induced caecs.Mtt, hoechst 33258 staining, and tube formation assay were employed in order to measure cell viability, apoptosis, and tube formation, respectively.The levels of il‐1β, il‐6, il‐10, and il‐18 were determined by elisa.Il1r2 was verified as the target gene of mi r‐383‐3p by dual‐luciferase reporter gene assay.Mi r‐383‐3p was down‐regulated in myocardial tissues of as rats while il1r2 was the reciprocal.The up‐regulation of mi r‐383‐3p decreased the levels of il1r2, caspase‐1, il‐1β, il‐6, and il‐18 expressions, as well as cell apoptosis rate in the hcy‐induced caecs, while il‐10 expression, cell viability, and tube formation ability were increased.These results were contraindicated in the hcy‐induced caecs treated by mi r‐383‐3p inhibitors.In conclusion, mi r‐383‐3p mediating il1r2 prevents hcy‐induced apoptosis and inflammation injury in caecs through the inhibition of the activation of inflammasome signaling pathway.These findings highly indicate that mi r‐383‐3p may be beneficial in the prevention of cas and other cardiovascular diseases.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
RNA interference-mediated silencing of S100B improves nerve function recovery and inhibits hippocampal cell apoptosis in rat models of ischemic stroke

Ischemic stroke is the leading cause of worldwide mortality and long‐term disability in adults.This study aims to explore the effects of rna interference (rnai)‐mediated silencing of the s100b gene on nerve function recovery and morphological changes of hippocampus cells in rat models with ischemic stroke.Sixty wistar rats were assigned into different group.S100b and caspase 3 m rna and protein expressions were evaluated by rt‐q pcr and western blotting.Positive rate of s100b, neu n, and map2 expressions were detected by immunohistochemistry (ihc).Water content, malondialdehyde (mda) levels, and superoxide dismutase (sod) activity in brain tissues were measured.Enzyme‐linked immunosorbent assay (elisa) was employed to detect serum levels of tnf‐α and il‐1β.A neurological severity score (nss) was used to test nerve function.Tunel assay was used to determine hippocampal cell apoptosis.Downregulation of s100b showed a lower number of s100b immune positive cells, but higher neu n and map2‐positive cells, increased sod level, declined mda level, prominently faster recovery of neurological function, decreased trcs, tctp, tcfp, and ie levels, an obvious increase in the number of survival neurons, a decrease in the number of apoptotic cells, notably decreased tnf‐α and il‐1β contents, as well as infarct volume, an obvious decrease in positive hippocampal cell caspase 3 expression and protein expressions of caspase 3 and cleaved caspase 3.This study provides data to suggest that rnai‐mediated silencing of s100b gene could improve the recovery of nerve function while inhibiting apoptosis of hippocampal cells in rats with ischemic stroke.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Upregulation of Klotho potentially inhibits pulmonary vascular remodeling by blocking the activation of the Wnt signaling pathway in rats with PM2.5-induced pulmonary arterial hypertension

We evaluated the effects of klotho on pulmonary vascular remodeling and cell proliferation and apoptosis in rat models with pm2.5‐induced pulmonary arterial hypertension (pah) via the wnt signaling pathway.After establishing rat models of pm2.5‐induced pah, these sprague‐dawley male rats were randomized into control and model groups.Cells extracted from the model rats were sub‐categorized into different groups.Activation of wnt/β‐catenin signaling transcription factor was detected by a topflash/fopflash assay.A serial of experiment was conducted to identify the mechanism of klotho on pha via the wnt signaling pathway.Vegf levels and pa co 2 content were higher in the model group, while pa o 2, no 2 − /no 3 − content and klotho level was lower compared to the control group.In comparison to the control group, the model group had decreased klotho and bax levels, and elevated wnt‐1, β‐catenin, bcl‐2, survivin, and pcna expression, vegf, il‐6, tnf‐α, tnf‐β1, and b fgf levels, as well as the percentage of pulmonary artery ring contraction.The klotho vector, dkk‐1 and dkk‐1 + klotho vector groups exhibited reduced cell proliferation, luciferase activity, and the expression of wnt‐1, β‐catenin, bcl‐2, survivin, and pcna, as well as shortened s phase compared with the blank and nc groups.Compared with the klotho vector and dkk‐1 groups, the dkk‐1 + klotho vector groups had reduced cell proliferation, luciferase activity, and the expression of wnt‐1, β‐catenin, bcl‐2, survivin, and pcna, as well as a shortened s phase.Conclusively, klotho inhibits pulmonary vascular remodeling by inactivation of wnt signaling pathway.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
microRNA-129-5p involved in the neuroprotective effect of dexmedetomidine on hypoxic-ischemic brain injury by targeting COL3A1 through the Wnt/β-catenin signaling pathway in neonatal rats

Our study aims to elucidate the mechanisms how micro rna‐129‐5p (mi r‐129‐5p) involved in the neuroprotective effect of dexmedetomidine (dex) on hypoxic‐ischemic brain injury (hibi) by targeting the type iii procollagen gene (col3a1) through the wnt/β‐catenin signaling pathway in neonatal rats.A total of 120 rats were obtained, among which 15 rats were selected as sham group and rest rats as model, dex, dex + negative control (dex + nc), dex + mi r‐129‐5p mimics, dex + mi r‐129‐5p inhibitors, dex + xav‐939, and dex + mi r‐129‐5p inhibitors + xav‐939 groups.A dual‐luciferase reporter assay was performed for the target relationship between mi r‐129‐5p and col3a1.Weight rate and water content of cerebral hemisphere were detected.Quantitative real‐time polymerase chain reaction and western blot analysis were conducted to detect mi r‐129‐5p expression and expressions of col3a1, e‐cadherin, t‐cell factor (tcf)− 4, and β‐catenin.The dex, dex + mi r‐129‐5p mimics, dex + xav‐939 groups had increased weight rate of the cerebral hemisphere, but decreased water content of left cerebral hemisphere, levels of col3a1, β‐catenin, tcf‐4, and e‐cadherin in the hippocampus compared with the model and dex + mi r‐129‐5p inhibitors groups.Col3a1 was verified as the target gene of the mi r‐129‐5p.Compared with the dex + nc and dex + mi r‐129‐5p inhibitors + xav‐939 groups, the dex + xav‐939 and dex + mi r‐129‐5p mimics groups had elevated weight rate of the cerebral hemisphere, but reduced water content of left cerebral hemisphere, levels of col3a1, β‐catenin, tcf‐4, and e‐cadherin in the hippocampus.Our findings demonstrate that mi r‐129‐5p improves the neuroprotective role of dex in hibi by targeting col3a1 through the wnt/β‐catenin signaling pathway in neonatal rats.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Protective effects of microRNA-330 on amyloid β-protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

This study aims to explore the effect of mi r‐330 targeting vav1 on amyloid β‐protein (aβ) production, oxidative stress (os), and mitochondrial dysfunction in alzheimer's disease (ad) mice through the mapk signaling pathway.Putative targeted gene of mi r‐330 was performed by a mi rna target prediction website and dual‐luciferase reporter gene assay.Ad mouse model was successfully established.Fourteen c57 mice were randomized into ad and control groups.The positive protein expression rate of vav1 was measured by immunohistochemistry.Neuron cells were assigned into control, blank, negative control (nc), mi r‐330 mimics, mi r‐330 inhibitors, si rna‐vav1, and mi r‐330 inhibitors + si rna‐vav1 groups.Expression of mi r‐330, vav1, erk1, jnk1, p38mapk, aβ, cox, and lipoprotein receptor‐related protein‐1 (lrp‐1) were determined using rt‐q pcr and western blotting.Colorimetry was applied to measure the levels of os parameters of superoxide dismutase (sod) and malondialdehyde (mda).Aβ production in brain tissue was detected using elisa, while that in neuron cell was measured by radioimmunoassay.Mi r‐330 was down‐regulated in neuron cells of ad mice and vav1 was negatively regulated by mi r‐330.Compared with the control group, the positive protein expression rate of vav1 was significantly elevated in the ad group.Overexpression of mi r‐330 decreased the expression of vav1, erk1, jnk1, p38mapk, and aβ, but increased the expression of cox and lrp‐1.Ad mice revealed elevated aβ production and mda with decreased sod level.The result indicates that overexpressed mi r‐330 targeting vav1 through the mapk signaling pathway reduces aβ production and alleviates os and mitochondrial dysfunction in ad.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
MicroRNA-335-5p suppresses lower extremity deep venous thrombosis by targeted inhibition of PAI-1 via the TLR4 signaling pathway

This study aims to investigate the effects of micro rna‐335‐5p (mi r‐335‐5p) on lower‐extremity deep vein thrombosis (ledvt) by targeting pai‐1 through the tlr4 signaling pathway in rat models.Si rna, mimic, and inhibitor were used for transfection.The mi r‐335‐5p expression was detected by in situ hybridization.Cck‐8 assay and flow cytometry were adopted to detect proliferation, cell cycle, and apoptosis, respectively.Scratch test and matrigel‐based tube formation assay were used to detect the effect of mi r‐335‐5p on cell migration ability and tube formation ability.A mi r‐335‐5p lentivirus plasmid was constructed and injected into ledvt rats.The length and weight of thrombus were measured, changes of thrombus recanalization were observed by cd34 immunohistochemistry, and levels of pai‐1 and inflammatory factors in femoral vein blood were detected by elisa.Ledvt rats showed a higher aod value of pai‐1, higher expression of pai‐1, nf‐κb, rac1, il‐1β, and tlr4 and a lower mi r‐335‐5p expression.Pai‐1 and mi r‐335‐5p were negatively correlated.Compared to the blank and si rna‐nc groups, the mi r‐335‐5p mimic and si rna‐pai‐1 groups showed declined expression of pai‐1, tlr4, nf‐κb, rac1, and il‐1β, increased proliferation and tube formation abilities, less cells in g0/g1 phase, and decreased apoptosis, decreased length and weight of thrombus, organized thrombus, increased new blood vessels, and decreased levels of pai‐1, il‐1, il‐6, and tnf‐a.Mi r‐335‐5p may suppress the occurrence and development of ledvt in rats by repressing the activation of the tlr4 signaling pathway by targeted inhibition of pai‐1.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
CUL4B promotes metastasis and proliferation in pancreatic cancer cells by inducing epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway

This study determines whether cullin 4b (cul4b) promotes pancreatic cancer (pc) metastasis by inducing epithelial‐mesenchymal transition (emt) via the wnt/β‐catenin signaling pathway.A total of 64 pc patients were enrolled in this study.Human pc cell lines were distributed into blank, negative control, sh cul4b, ploc, ploc‐cul4b, and ploc‐cul4b + si rna‐β‐catenin groups.The expressions of cul4b, wnt/β‐catenin signaling pathway‐related proteins, and emt‐related proteins were determined using rt‐q pcr and western blotting.The positive expressions of cul4b and β‐catenin protein in tissues were detected by immunohistochemistry.Mtt assay and flow cytometry was performed for cell proliferation and cell cycle, scratch test, and transwell assay for cell migration and invasion ability.Cul4b and β‐catenin were expressed at a higher level in pc tissues than in paracancerous tissues though paracancerous tissues had higher expressions of cul4b and β‐catenin than normal tissues.The ploc‐cul4b group showed increased cul4b, wnt, β‐catenin, lef‐1, c‐jun, cyclin d1, n‐cadherin, vimentin, snail, and zeb1 expression; decreased e‐cadherin expression; accelerated cell proliferation; increased s‐phase cell percentages; increased cell migration ability; more liver metastases; and enlarged tumor than the ploc and ploc‐cul4b + si rna‐β‐catenin groups.The sh cul4b group showed decreased cul4b, wnt, β‐catenin, lef‐1, c‐jun, cyclin d1, n‐cadherin, vimentin, snail, and zeb1 expression; increased e‐cadherin expression; decelerated cell proliferation; decreased s‐phase cell percentages; reduced cell migration ability; less liver metastases; and decreased tumor weight than the blank and negative control groups.We demonstrate that cul4b promotes pc metastasis by inducing emt via the wnt/β‐catenin signaling pathway.Therefore, cul4b might be the clinical target for treating pc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Evaluation of the circulating MicroRNA-495 and Stat3 as prognostic and predictive biomarkers for lower extremity deep venous thrombosis

This study aims to elucidate the prognostic and predictive biomarker of mi r‐495 and stat3 in peripheral blood in relation to lower extremity deep venous thrombosis (dvt).Patients with lower limb fractures were assigned into case and control groups.Rats were allocated into blank (normal rats), sham (normal rats), dvt, mi r‐495 mimic, mi r‐495 inhibitor, over‐stat3, and si‐stat3 groups.Elisa was used to detect levels of prothrombin time (pt), endothelin‐1 (et‐1), human fibrinogen (fib), d‐dimer, blood coagulation factors v and viii, tissue type plasminogen activator (t‐pa), platelet activating factor (paf), protein c and stat3.Q rt‐pcr was employed for the evaluation of the expressions of mi r‐495 and stat3, while receiver operating characteristic (roc) curve was constructed to assess the predictive value of mi r‐495 and stat3 as well as the treatment outcomes of patients with lower limb fractures.Logistic regression analyses were conducted in order to correlate indexes and lower extremity dvt.Mi r‐495 overexpression, t‐pa, paf, and protein c were confirmed to be protective factors, while stat3 overexpression, pt, et‐1, fib, d‐dimer, blood coagulation factor v, and viii were all ultimately considered to be risk factors of lower extremity dvt.Stat3 was confirmed to be the target gene of mi r‐495.Compared with the blank group, the length and weight of the thrombus as well as the ratio between length and weight, m rna and protein expression of stat3 were reduced in the mi r‐495 mimic and si‐stat3 groups.Our findings suggest that through the suppression of stat3 expression, mi r‐495 prohibits lower extremity dvt in peripheral blood.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;