syedzayyan/paper_mill_benchmark huggingface dataset:
Inhibition of SNK-SPAR signaling pathway promotes the restoration of motor function in a rat model of ischemic stroke

This study aimed to investigate the effects of spar signaling pathway on the restoration of motor function in ischemic stroke (is).Sprague‐dawley male rats were separated into the control and sham groups, as well as the group for middle cerebral artery occlusion (mcao) model establishment.Successfully established rat ischemic models were randomly divided into model, snk mcao‐del and pc dna3.1‐snk groups.The evaluation of motor function among the rats in each group was assessed using a balance beam, a screen test and the garcia scoring method.Cat walk gait analysis was employed to evaluate the effect of the snk signaling pathway on rat motor function.Triphenyltetrazolium chloride (ttc) and tunel staining were techniques were utilized for cerebral infarction (ci) area as well for hippocampal neuron apoptosis.The quantitative real‐time polymerase chain reaction (q rt‐pcr) and western blotting methods were performed to detect m rna and protein expressions of snk and spar.When compared with the model group, the snk mcao‐del group displayed decreased motor function score and ci area, while contrasting results were observed in the pc dna3.1‐snk group.According to the results obtained from the cat walk gait analysis, the snk mcao‐del group showed a clear improvement compared to the model group whereas the pc dna3.1‐snk group exhibited poorer results than the model group in the objective parameters of the study, such as movement, speed, running duration, print area, maximal contact area, maximal, mean intensity, and stride length.These findings suggested that snk gene silencing promotes motor function by inhibiting the snk‐spar signaling pathway in rats with ischemic stroke.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
MicroRNA-300 promotes apoptosis and inhibits proliferation, migration, invasion and epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway by targeting CUL4B in pancreatic cancer cells

The study aims to verify the hypothesis that up‐regulation of micro rna‐300 (mi r‐300) targeting cul4b promotes apoptosis and suppresses proliferation, migration, invasion, and epithelial‐mesenchymal transition (emt) of pancreatic cancer cells by regulating the wnt/β‐catenin signaling pathway.Pancreatic cancer tissues and adjacent tissues were collected from 110 pancreatic cancer patients.Expression of mi r‐300, cul4b, wnt, β‐catenin, e‐cadherin, n‐cadherin, snail, gsk‐3β, and cyclin d1 were detected using q rt‐pcr and western blot.Cfpac‐1, capan‐1, and panc‐1 were classified into blank, negative control (nc), mi r‐300 mimics, mi r‐300 inhibitors, si rna‐cul4b, and mi r‐300 inhibitors + si rna‐cul4b groups.The proliferation, migration, invasion abilities, the cell cycle distribution, and apoptosis rates were measured in cck‐8 and transwell assays.Pancreatic cancer tissues showed increased cul4b expression but decreased mi r‐300 expression.When mi r‐300 was lowly expressed, cul4b was upregulated which in‐turn activated the wnt/β‐catenin pathway to protect the β‐catenin expression and thus induce emt.When mi r‐300 was highly expressed, cul4b was downregulated which in‐turn inhibited the wnt/β‐catenin pathway to prevent emt.Weakened cell migration and invasion abilities and enhanced apoptosis were observed in the cul4b group.The mi r‐300 inhibitors group exhibited an evident increase in growth rate accompanied the largest tumor volume.Smaller tumor volume and slower growth rate were observed in the mi r‐300 mimics and si rna‐cul4b group.Our study concludes that lowly expressed mi r‐300 may contribute to highly expressed cul4b activating the wnt/β‐catenin signaling pathway and further stimulating emt, thus promoting proliferation and migration but suppressing apoptosis of pancreatic cancer cells.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
microRNA-145-3p inhibits non-small cell lung cancer cell migration and invasion by targeting PDK1 via the mTOR signaling pathway

The mammalian target of rapamycin (m tor) pathway is dysregulated in more than 50% of all human malignancies and is a major target in cancer treatment.In this study, we explored the underlying mechanism involving micro rna‐145‐3p (mi r‐145‐3p) in the development and progression of non‐small cell lung cancer (nsclc) by targeting pdk1 via the m tor signaling pathway.Nsclc tissues and adjacent normal tissues were obtained from 83 nsclc patients.Mi r‐145‐3p, pdk1, and m tor levels were determined by quantitative real‐time polymerase chain reaction (q rt‐pcr) and immunohistochemistry.Human nsclc cell lines a549 and h1299 were transfected with mi r‐145‐3p and si pdk1 to confirm the effect of mi r‐145‐3p and pdk1 on nsclc cells in vitro.Cell growth was evaluated by a cck8 assay.Cell motility and chemotaxis analysis were determined by the scratch test and chemotaxis assay, respectively.The protein levels of pdk1 and m tor were measured using the western blotting.Results showed lower level of mi r‐145‐3p and higher levels of pdk1 and m tor in nsclc tissues compared to the adjacent normal tissues.In vitro results showed that cell growth, cell motility, and chemotaxis were all inhibited in cells transfected with mi r‐145‐3p and those transfected with si pdk.Additionally, dual luciferase reporter gene assay helped confirmed that pdk1 is a target of mi r‐145.Finally, levels of pdk1, m tor, and phosphorylated‐m tor were lower in cells transfected with mi r‐145‐3p as well as those with si pdk1.These findings indicate that mi r‐145‐3p may inhibit cell growth, motility, and chemotaxis in nsclc by targeting pdk1 through suppressing the m tor pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of astragalus polysaccharide on apoptosis of myocardial microvascular endothelial cells in rats undergoing hypoxia/reoxygenation by mediation of the PI3K/Akt/eNOS signaling pathway

The study explores the effect of astragalus polysaccharide (aps) mediating p13k/akt/e nos signaling pathway on apoptosis of myocardial microvascular endothelial cells (mmecs) in hypoxia/reoxygenation (h/r).Mmecs were classified into blank, h/r, h/r + 25 mg/l aps, h/r + 50 mg/l aps, h/r + 100 mg/l aps, h/r + ly, and hr + 100 mg/l aps + ly groups.Cell viability was detected using mtt assay and apoptotic cell morphological changes by hoechst staining.No content, cell cycle and apoptosis, pi3k/akt/e nos signaling pathway proteins were detected using nitrate reductase assay, flow cytometry and western blotting.An increased cell survival rate, no content and expression of pi3k/akt/e nos signaling pathway associated proteins, and a decreased apoptosis rate was observed in the h/r + 50 mg/l aps and h/r + 100 mg/l aps groups compared with the h/r and h/r + 25 mg/l aps groups.Compared with the h/r + 50 mg/l aps group, the apoptosis rate decreased, whereas the cell survival rate, no content and expression of pi3k/akt/e nos signaling pathway associated proteins increased in the h/r + 100 mg/l aps group.The h/r + ly and hr + 100 mg/l aps + ly groups followed opposite trends.In comparison to the hr + 100 mg/l aps group, the apoptosis rate in the h/r + ly and hr + 100 mg/l aps + ly groups increased, and the cell survival rate, no content and expression of pi3k/akt/e nos signaling pathway associated proteins decreased.Collectively, aps improves the damage caused by h/p by mediating pi3k/akt/e nos signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
The Role of MicroRNA-143-5p in the Differentiation of Dental Pulp Stem Cells into Odontoblasts by Targeting Runx2 via the OPG/RANKL Signaling Pathway

This study aims to elucidate the mechanisms by which micro rna‐143‐5p (mi r‐143‐5p) targets runt‐related transcription factor 2 ( runx2 ) in the differentiation of dental pulp stem cells (dpscs) into odontoblasts, through regulating the osteoprotegerin receptor activator of the nuclear factor‐κb ligand ( opg / rankl ) signaling pathway.Following transfection, dpscs were divided into blank, control, mi r‐143‐5p mimics, mi r‐143‐5p inhibitors, mi r‐143‐5p inhibitors + si runx2 and si runx2 groups.Alkaline phosphatase (alp) activity and mineralized nodules were detected using alp kit and alizarin red staining.Quantitative reverse transcriptase real time pcr (q rt‐pcr) was conducted to measure m rna expressions of mi r‐143‐5p, runx2 , opg , and rankl .Western blotting was used to assess protein expression of odontoblast differentiation‐related proteins.Transwell assay and an extracellular matrix (ecm) adhesion cell assay were employed to examine cell migration and cell adhesion.Compared with the blank group, the mi r‐143‐5p mimics and si runx2 groups showed decreased alp activity, decreased mineralized nodules and displays of calcium.Fewer migrated cells, weakened cell adhesion, decreased protein expression of dentin phosphoprotein (dpp), dentin sialoprotein (dsp), dentin matrix protein 1 (dmp1), osteopontin (opn), bone sialoprotein (bsp), osteocalcin (ocn), opg and runx2, and increased rankl protein expressions were observed.Additionally, opposite results were observed in the mi r‐143‐5p inhibitors group, demonstrating that down‐regulated mi r‐143‐5p promotes the differentiation of dpscs into odontoblasts by enhancing runx2 expression via the opg / rankl signaling pathway.Based on findings in this study, it is postulated that the enhancement of runx2 expression via the regulation of the opg / rankl signaling pathway could be a beneficial approach for dental pulp regeneration.J.Cell.Biochem.119: 536–546, 2018.© 2017 wiley periodicals, inc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Cyclin D1 Gene Silencing Promotes IL-1β-Induced Apoptosis in Rat Chondrocytes

This study investigated the effects of cyclin d1 gene silencing on cell proliferation and apoptosis of interleukin‐1β (il‐1β)‐induced osteoarthritis (oa) chondrocytes.Chondrocytes from healthy sprague‐dawley rats were divided into blank, oa model (chondrocytes underwent il‐1β inducement), oa trial (chondrocytes underwent il‐1β inducement with cyclin d1‐sh rna treatment), and negative control (nc; chondrocytes underwent il‐1β inducement and control‐sh rna treatment) groups.Cell proliferation was assessed by cck‐8 assay, and cell cycle and apoptosis by flow cytometry.Q rt‐pcr and western blotting were performed to detect cyclin d1 and apoptosis‐related factors expression levels.Chondrocyte proliferation increased after 72–96 h after incubation.The oa trial group exhibited reduced cell proliferation at 48, 72, and 96 h after treatment.The oa model, oa trial, and nc groups all contained more cells arrested in g1 phase and had higher apoptosis rates than the blank group.Additionally, the oa trial group contained more cells arrested in g1 phase, with increased apoptosis rates compared to the oa model and nc groups.The oa model group had lowest expression of cyclin d1 whereas the blank group contained the highest among the four groups.Q rt‐pcr also showed that the oa model, oa trial, and nc groups all had increased expression levels of bax and reduced expression levels of bcl‐2 and p53 compared to the blank group, whereby by the oa group had the most significant change.The combined evidence in our study shows that cyclin d1 gene silencing suppresses proliferation and induces apoptosis of rat chondrocytes in il‐1β‐induced oa.J.Cell.Biochem.119: 290–299, 2018.© 2017 wiley periodicals, inc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of shRNA-Mediated Silencing of PKM2 Gene on Aerobic Glycolysis, Cell Migration, Cell Invasion, and Apoptosis in Colorectal Cancer Cells

This study aims to explore the effects of sh rna‐mediated silencing on pyruvate kinase type m2 (pkm2) gene during aerobic glycolysis in colorectal cancer (crc) cells.Crc tissues and adjacent normal tissues were obtained from 136 patients diagnosed with q rt‐pcr, western blotting, and immunohistochemistry (ihc) were performed to detect m rna and protein expressions of pkm2.Crc cells were divided into a blank, vector, and pkm2‐sh rna groups.Hexokinase (hk) and pkm2 activity were both determined by glucose‐6‐phosphate dehydrogenase (g‐6‐pd) coupled colorimetric assay and enzyme coupling rate method.The extracellular lactate concentration was measured by ultraviolet spectrophotometer and caspase activity was measured using spectrophotometry.The proliferation, cell cycle, apoptosis, invasion, and migration of crc cells were detected by cell counting kit‐8 (cck‐8) assay, flow cytometry, transwell assay, and scratch test.Three groups of nude mice were injected with 0.2 m l single‐cell suspension from the blank, vector, and pkm2‐sh rna groups, respectively.Pkm2 protein content in crc tissues was higher than that in adjacent normal tissues.Results showed that the pkm2‐sh rna group exhibited significantly lower m rna and protein expressions of pkm2, decreased pkm2 activity, reduced lactate metabolism level, increased cell apoptosis rate, elevated caspase‐3 and caspase‐9 activity, weakened proliferation, and a reduction in cell invasion and migration ability compared to the vector and blank groups.The optical density (od) value was lower in the pkm2‐sh rna group than in the blank and vector groups.These findings indicate that sh rna‐mediated silencing of pkm2 gene promotes apoptosis and inhibits aerobic glycolysis, proliferation, migration, and invasion in crc cells.J.Cell.Biochem.118: 4792–4803, 2017.© 2017 wiley periodicals, inc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Activation of the Nrf2-ARE Signaling Pathway Prevents Hyperphosphatemia-Induced Vascular Calcification by Inducing Autophagy in Renal Vascular Smooth Muscle Cells

This study investigates the effect of nuclear factor erythroid 2‐related factor 2‐antioxidant response element (nrf2‐are) signaling pathway in vascular calcification (vc) via inducing autophagy in renal vascular smooth muscle cells (vsmcs).Vsmcs were assigned into six experimental groups: the normal control, high phosphorus, si‐negative control (si‐nc), nrf2‐si rna, over‐expressed nrf2, and negative control (nc) groups.Rt‐pcr was applied to detect the m rna expressions of the desired nrf2‐are signaling pathway‐related genes (nrf2, nqo‐1, ho‐1, γ‐gcs).The protein products of these genes: apoptosis‐related genes (lc3i and lc3ii), osteogenic marker proetins (runt‐related transcription factor 2) runx2 and bmp2 were all detected by western blotting.Autophagosomes in vsmcs were observed under a transmission electron microscope.We discovered an increased calcium ion concentration and upregulated runx2, bmp2, nrf2, ho‐1, γ‐gcs, nqo‐1, and lc3ii/lc3i expressions in the high phosphorous, si‐nc and nrf2‐si rna, and nc groups, compared with the normal control group.Compared to the high phosphorus and si‐nc groups, higher levels of runx2 and bmp2 but decreased nrf2, ho‐1, γ‐gcs, nqo‐1, and lc3ii/lc3i expressions were detected in the nrf2‐si rna group.The high phosphorus, si‐nc and over‐expressed nrf2 experimental groups all had increased nrf2, nqo‐1, ho‐1, γ‐gcs, and lc3ii/lc3i expressions as well as high numbers of autophagosomes compared with the normal control group.Finally, we detected a lower amount of autophagosomes presence and nrf2, nqo‐1, ho‐1 γ‐gcs, and lc3ii/lc3 protein expression of nrf2‐si rna group than that of the high phosphorus and si‐nc groups.Activation of nrf2‐are signaling pathway may prevent hyperphosphatemia‐induced vc by inducing autophagy in vsmcs.J.Cell.Biochem.118: 4708–4715, 2017.© 2017 wiley periodicals, inc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of MicroRNA-19b on the Proliferation, Apoptosis, and Migration of Wilms' Tumor Cells Via the PTEN/PI3K/AKT Signaling Pathway

Wilms’ tumor (wt) is a most common renal cancer that occurs among children, and micro rna‐19b (mi r‐19b) usually participates in various human cancers.Importantly, the pten/pi3k/akt signaling pathway plays a key role in cell apoptosis, growth and proliferation.Thus, our present study aims to investigate the effect of mi r‐19b on the pten/pi3k/akt signaling pathway during wt cell proliferation, migration, and apoptosis.Wt tissues and adjacent normal tissues from wt patients were collected.Q rt‐pcr was applied to detect mi r‐19b expression in both the wt tissues and the adjacent normal tissues, immunohistochemistry was applied to detect the protein expressions of pten, p13k, and p‐akt, sk‐nep‐1 cells were divided into the blank, negative control (nc), mi r‐19b mimics and mi r‐19b inhibitors groups.Mtt assay, propidium iodide (pi) staining, annexin‐v/pi double‐staining, transwell assay and western blotting were performed to examine cell proliferation, cycle, apoptosis, migration, and invasion, and the protein expressions of pten, p13k, akt, and p‐akt.Increased mi r‐19b expression, positive expression rates of p13k and akt, decreased pten expression rate, a negative correlation between pten expression and tumor lymph node metastasis, and a positive correlation between the expression of p13k and akt and the clinical stages were observed in the wt tissues.The mi r‐19b inhibitors group exhibited decreased cell proliferation, cell cycle progression, migration and invasion, and protein expressions of pi3k and p‐akt but increased pten protein expression compared with the blank and nc groups.Thus, inhibition of mi r‐19b suppresses the progression of wt by modulating the pten/pi3k/akt signaling pathway.J.Cell.Biochem.118: 3424–3434, 2017.© 2017 wiley periodicals, inc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

Background: long non-coding rna taurine up-regulated gene 1 (tug1) was reportedly involved in initiation and development of several cancers.However, its function and molecular mechanisms in multiple myeloma (mm) are still unclear.The present study aimed to determine the expression status, biological function, and potential mechanisms of tug1 in the progression of mm.Materials and methods: the expression levels of tug1 were examined in mm samples and cell lines by real-time quantitative pcr.The effects of tug1 on mm cells proliferation and apoptosis were assessed using cell counting kit-8 assay and flow cytometry respectively.Mi rnas-targeted sites in tug1 were screened by starbase2.0 and were identified by rna immunoprecipitation assay combined with luciferase reporter assay.Results: the expression levels of tug1 were markedly increased in mm samples and cell lines.Knockdown of tug1 significantly suppressed the proliferation, induced cell cycle arrest at g1/g0 phase, and promoted apoptosis of mm cells.In exploring the regulatory mechanism, mi r-29b-3p was confirmed to be a direct target of tug1, and repression of mi r-29b-3p could partially rescue the effect tug1 knockdown on mm cell proliferation, cycle, and apoptosis.In addition, tug1 positively modulated histone deacetylases 4 (hdac4, a target of mi r-29b-3p) expression through sponging of mi r-29b-3p in mm cells.Conclusion: these findings suggested that tug1 exerted an oncogenic role in mm by acting as a competing endogenous rna of mi r-29b-3p, and implied the potential application of tug1 in treatment for mm.

Journal: Bioscience Reports (2019)
Publication types: Research Article;
Protective effect of autophagy on endoplasmic reticulum stress-induced apoptosis of alveolar epithelial cells in rat models of COPD

During the present study, we explored the protective effects of autophagy on endoplasmic reticulum (er) stress (ers) induced apoptosis belonging to alveolar epithelial cells (aecs) in rat models with chronic obstructive pulmonary disease (copd).Fifty-six 12-week-old male sprague–dawley (sd) rats were randomly assigned into the copd group (rats exposed to cigarette smoke (cs)), the 3-methyladenine (3-ma) intervention group (copd rats were administrated with 10 mg/kg autophagy inhibitors), the chloroquine (cq)-intervention group (copd rats were administrated 40 mg/kg cq), and the control group (rats breathed in normal saline).The forced expiratory volume in 0.3 s/forced vital capacity (fev0.3/fvc%), inspiratory resistance (ri), and dynamic lung compliance (cdyn) were measured and recorded.The expressions of pkr-like er kinase (perk) and ccaat/enhancer-binding protein-homologous protein (chop) were detected by immunohistochemistry.The cell apoptotic rates of aecs were analyzed by terminal deoxynucleotidyl transferase (td t) mediated d utp-biotin nick end-labeling (tunel) staining.The expression levels of light chain 3 (lc3-ii), p62, beclin-1, atg5, atg7, caspase-12, and caspase-3 were detected by western blotting.Results showed that the copd group exhibited a lower fev0.3/fvc% and cdyn, and a higher ri than the control group.Compared with the control group, the integrated optical density (iod) values of perk and chop, the apoptotic rate of aecs, and expressions of lc3-ii, beclin-1, atg5, atg7, caspase-3, and caspase-12 expressions were significantly higher, whereas p62 expression was significantly lower in the copd group.Based on the results obtained during the present study, it became clear that the inhibition of autophagy could attenuate the ers-induced apoptosis of aecs in rats with copd.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
Long noncoding RNA MEG3 deteriorates inflammatory damage by downregulating microRNA-101a

Valvulopathy is a familiar heart disease, which fearfully harms the health of the body.We studied the effects and mechanism of long noncoding rna maternally expressed gene 3 (lnc meg3) on mvics cell in inflammatory damage.Cell counting kit‐8 and flow cytometry were respectively used to detect the effect of tumor necrosis factor α (tnf‐α), meg3 and micro rna (mi r)‐101a on cell viability and apoptosis.Moreover, meg3 and mi r‐101a expression were changed by cell transfection and investigated by reverse transcription‐quantitative polymerase chain reaction.Furthermore, western blot was used to investigate the levels of bax, pro‐caspase‐3, cleaved‐caspase‐3, pro‐caspase‐9, cleaved‐caspase‐9, interleukin (il)‐1β, il‐6 and related‐proteins of cell pathways.Otherwise, the levels of il‐1β and il‐6 were also investigated by enzyme‐linked immunosorbent assay kit.Reactive oxygen species (ros) was examined by ros assay.We found tnf‐α caused inflammatory damage and upregulated meg3.Meg3 was overexpressed and silenced in cells.Besides, meg3 deteriorated inflammatory damage.Furthermore, meg3 negatively regulated mi r‐101a and mi r‐101a mimic could reverse the effect of pc‐meg3.Besides, meg3 enhanced the jnk and nf‐κb pathways by downregulating mi r‐101a.In conclusion, meg3 deteriorated cell inflammatory damage by downregulating mi r‐101a via jnk and nf‐κb pathways.

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