syedzayyan/paper_mill_benchmark huggingface dataset:
Prognostic significance of long non-coding RNA MALAT1 for predicting the recurrence and metastasis of gallbladder cancer and its effect on cell proliferation, migration, invasion, and apoptosis

The objective of this study is to explore the role of malat1 as a molecular indicator in predicting the recurrence, metastasis, and prognosis of gallbladder cancer (gbc) and its effect on the proliferation, invasion, migration, and apoptosis of gbc cells in vitro.Gbc tissues and adjacent normal tissues were collected from 102 patients.Malat1 short hairpin rna (sh rna) plasmids were first constructed to transfect the gbc‐sd cells.Reverse transcription quantitative polymerase chain reaction (rt‐q pcr) was applied to detect malat1 expression.Cck‐8 assay, flow cytometry, and transwell assay were applied to testify the cell proliferation, cell cycle, apoptosis, invasion, and migration.A receiver operating characteristic (roc) curve was used to evaluate the values of malat1 in gbc recurrence, metastasis, and prognosis.Cox regression analysis was applied to analyze the independent influencing factors of gbc patients’ survival status.Roc curve results showed that the malat1 expression could be a predictor of the gbc recurrence, metastasis, and prognosis.According to the cox regression analysis, malat1 expression, tumor size, and tnm stage were independent influencing factors of gbc patients’ survival condition.Compared with the gbc‐sd cells transfected with empty plasmids, those transfected with malat1 sh rna plasmids showed higher apoptosis rates, weakened proliferation, migration, and invasion.In conclusion, our findings demonstrate that lnc rna malat1 can be considered as an indicator for evaluating the recurrence, metastasis, and prognosis of gbc patients.We also demonstrate how the overexpression of malat1 confers an oncogenic function in gbc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
In vivo and in vitro effects of microRNA-124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway

In this study, we aim to determine the function of mi r‐124 on gastric cancer (gc) cells and the underlying mechanism that involves jaddeg1 (jag1) and the notch signaling pathway.Gc tissues and adjacent tissues from 100 patients suffering from gc were selected.Gc sgc‐7901 and ags cells were selected and grouped into control, mimic‐nc, mi r‐124 mimic, inhibitor‐nc, mi r‐124 inhibitor, and mi r‐124 inhibitor + si‐jag1 groups.Rt‐q pcr and a western blotting assay were conducted to detect the expression of mi r‐124, jag1, and notch signaling pathway‐related proteins (nicd, hes1, and hes5).Mts, wound‐healing, transwell assay and flow cytometry were performed to detect cell proliferation, migration, invasion, cell cycle distribution, and apoptosis, respectively.Compared with adjacent tissues, a lower mi r‐124 expression and higher jag1 expression were found in gc tissues.Jag1 is a direct target gene of mi r‐124.Compared with the control group, the expression of jag1, nicd, hes1, and hes5, cell invasion, migration, and proliferation in the mi r‐124 mimic group were decreased, while the apoptosis rate was increased and cells were arrested at the g0/g1 phase.Compared with the mi r‐124 inhibitor group, the expression of jag1, nicd, hes1, and hes5, cell invasion, migration, and proliferation in the mi r‐124 inhibitor + si‐jag1 group were decreased, while the apoptosis rate and cell ratio at the g0/g1 phase were increased.The demonstration that mi r‐124 inhibits gc cell growth supports the concept that mi r‐124 functions as a tumor suppressor by a mechanism that involves translational repression of the jag1 and the inhibition of notch signaling pathway.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of cyclin D1 gene silencing on cell proliferation, cell cycle, and apoptosis of hepatocellular carcinoma cells

This study aims to investigate the effects of cyclin d1 silencing on cell cycle, cell proliferation, and apoptosis of hepatocellular carcinoma cells (hcc).Cells were divided into the blank group, negative control group (hcc cells transfected with control sh rna), cyclin d1 sh rna group (hcc cells transfected with cyclin d1 sh rna), and the normal group (human normal liver l‐02 cells).Expressions of cyclin d1, caspase‐3, bcl‐2, and c‐myc were detected by rt‐q pcr and western blotting.Cell proliferation was detected by cell counting kit‐8.Cell cycle and apoptosis were detected by flow cytometry.Tumor xenograft in nude mice was performed to detect in vivo tumorigenesis.Hcc tissues and hcc cells exhibited elevated expression levels of cyclin d1.Cyclin d1 expression levels was found to be correlated with tumor size and tumor staging.Compared with the normal group, the blank group showed enhanced cell proliferation, a reduction in the amount of cells in g0/g1 phase, increased number cells in s and g2/m phase, reduced apoptosis, elevated expressions of cyclin d1, bcl‐2, and c‐myc, decreased caspase‐3 activity and significant tumorigenicity.In comparison with the blank group, the cyclin d1 sh rna group revealed weakened cell proliferation, reduced cells in s and g2/m phase, increased cells in g0/g1 phase, increased annexin v positive cell ratio, decreased expression of cyclin d1, bcl‐2, and c‐myc, elevated caspase‐3 activity and inhibited tumorigenicity.In conclusion, cyclin d1 gene silencing suppresses cell proliferation and inhibits cell apoptosis, which may be a new target approach in the treatment and management for hcc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Down-regulation of the long noncoding RNA-HOX transcript antisense intergenic RNA inhibits the occurrence and progression of glioma

This study aims to explore the role of long noncoding rna (lnc rna)‐hox transcript antisense intergenic rna (hotair) in the occurrence and progression of glioma.Fresh glioma and normal brain tissues were classified into a glioma group ( n = 67) and a normal group ( n = 64) respectively.U87 cells were assigned into the blank, sh‐nc, and sh‐hotair groups.Quantitative real‐time polymerase chain reaction (q rt‐pcr) was utilized to determine hotair expression.Cell proliferation, cell cycle and cell apoptosis rates were detected by cell counting kit‐8 (cck‐8) and flow cytometry (fcm).Scratch test and transwell assay were conducted for cell migration and invasion.Orthotopic glioma tumor model in nude mice was established by inoculating tumor cell suspension.Hematoxylin‐eosin (he) staining was used to observe the growth and invasion of orthotopic glioma tumors.The expression of hotair and cell viability was found to be lowest in the sh‐hotair group among the three groups.The sh‐hotair group exhibited a higher apoptotic rate and lower number of cell migration compared with the blank and sh‐nc groups.Additionally, the speed of wound healing was slower, the migration distance decreased and the survival time of nude mice was extended in the sh‐hotair compared to the other groups.Moreover, the sh‐hotair group demonstrated reduced lesion sizes and inflammation, no convulsions or hemiplegia and lesser number of satellite metastases.Our findings support that down‐regulation of hotair could inhibit cell proliferation, promote cell apoptosis as well as suppress cell invasion and migration in the progression of glioma.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Interleukin-6 promotes the migration and cellular senescence and inhibits apoptosis of human intrahepatic biliary epithelial cells

Biliary epithelial cells (bec) are closely related to some immune regulatory bile duct diseases.However, the complexity and polymorphism of the morphology and function of bile duct cells have hindered further investigation.Therefore, the aim of this study is to investigate how interleukin‐6 (il‐6) affects the migration, cellular senescence, and apoptosis of human intrahepatic biliary epithelial cells (hibecs).The hibecs were stimulated by different concentrations of il‐6 (0, 5, 10, 15, and 20 ng/m l, respectively).Transwell assay was performed in order to measure the migration abilities, positive β‐galactosidase staining for the cellular senescence of hibecs, mtt assay for changes of proliferation after il‐6 treatment and flow cytometry for cell cycle and apoptosis.The reverse transcription quantitative polymerase chain reaction (rt‐q pcr) and western blotting were conducted in order to detect the m rna and protein expressions of epithelial‐mesenchymal transition (emt) markers in hibecs.In comparison to the 0 ng/m l group, in the 5, 10, 15, and 20 ng/m l groups, a significant increase in the number of migratory hibecs, proliferation, along with m rna and protein expressions of emt markers was observed.While the m rna and protein expressions of epithelial markers, the number of β‐galactosidase positive staining cells, as well as apoptosis rate of hibecs dramatic decreased.Further, the aforementioned changes were significantly more evident in the 15 and 20 ng/m l groups in comparison to the 5 and 10 ng/m l groups.Il‐6 may stimulate emt, enhance the migration and proliferation, and inhibit apoptosis of hibecs, thus delaying cellular senescence.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Expression of nestin in embryonic tissues and its effects on clinicopathological characteristics of patients with placenta previa

In this study, we examined expression of nestin in the spinal cord, lung, kidney, stomach, colon, and intestine tissues at different stages of embryos in patients with placenta previa.Fetuses of 75 patients with placenta previa were assigned to case group and 80 fetuses from healthy pregnant women with normal placenta who voluntarily terminated pregnancy to control group.Clinical data of pregnant women were collected at the time of admission.Blood from elbow vein was collected to determine expression of serum nestin.Tissues from spinal cord, lung, kidney, stomach, colon, and intestine in 3‐7 months fetuses of the two groups were extracted.Expression of nestin in tissues was detected by immunohistochemistry, western blotting and rt‐q pcr.The m rna expression of nestin in the case group was increased.Nestin expression was correlated with the gestational age, age of foetus, and type of placenta previa in patients with placenta previa.Positive nestin expression was detected in the spinal cord, lung, kidney, stomach, intestine, and colon tissues in normal and placenta previa embryo at stage i.The positive cell density and nestin expression decreased at stage ii, and further decreased at stage iii.The case group had higher nestin m rna and protein levels throughout human fetal development.Findings of this study suggested that, nestin, as a specific marker of neural precursor cells, was expressed in various tissues of the embryo in patients with placenta previa and nestin expression was lower with increased maturation of the embryo.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Clinical Study;
Correlation of the expressions of IGF1R-RACK1-STAT3 and Bcl-xl in nasopharyngeal carcinoma with the clinicopathological features and prognosis of nasopharyngeal carcinoma

The aim of this study was to investigate the correlation of expression of igf1r‐rack1‐stat3 and bcl‐xl in nasopharyngeal carcinoma (npc) with the clinicopathological features and the prognosis of npc.Our study selected 215 npc tissues and 178 chronic nasopharyngitis tissues (control group).Positive expression rates of igf1r, rack1, stat3, and bcl‐xl were tested by immunohistochemical method, and expression of igf1r, rack1, stat3, bcl‐xl, bcl‐2, and bax by western blotting.Correlation of igf1r, rack1, stat3, and bcl‐xl with the clinicopathological features of npc was analyzed.The correlation among those four expression was analyzed by spearman.The survival of npc and independent factors of prognosis were tested by kaplan‐meier and cox proportional hazards model respectively.The npc group had higher positive expression rates of igf1r, rack1, stat3, and bcl‐xl, and elevated expression of igf1r, rack1, stat3, bcl‐xl, bcl‐2, and bax.The lymph node metastasis (lnm) group had higher positive expression rates of igf1r and rack1 when compared with the non‐lnm group.Patients with stage iii and iv had higher positive expression rates of igf1r, rack1, stat3, and bcl‐xl.There was positive correlation between expression of igf1r and rack1, stat3.Such correlation was found between rack1 and stat3.Patients with negative expression of igf1r, rack1, stat3, and bcl‐xl had higher survival rates.The risky factors of poor prognosis of npc were positive expression of igf1r, rack1, stat3 and bcl‐xl, and lnm.Igf1r‐rack1‐stat3 and bcl‐xl expression correlated with the clinicopathological features and poor prognosis of npc.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Circular RNA-0072309 has antitumor influences in Hep3B cell line by targeting microRNA-665

Liver cancer is a malignant tumor that occurs in the liver and has a high mortality rate.We strived to detect the role and mechanism of circ rna‐0072309 in liver cancer.Hep3b cell line was transfected with pc‐circ and si‐circ for viability, colony formation, apoptosis, migration, and invasion tests, which were individually performed by cck‐8, colony formation detection, flow cytometry assay, migration and invasion assays.What is more, the luciferase reporter assay was conducted to determine the target relationship between the circ rna‐0072309 and micro rna (mi r)‐665.The expression of circ rna‐0072309 was examined by q rt‐pcr.The expression of proteins was examined via western blot.Circ rna‐0072309 was lowly expressed in liver cancer tissues and positively associated with 5‐year survival rate.The viability, colony formation, invasive and migratory ability were inhibited by abundant circ rna‐0072309, which promoted cell apoptosis on the contrary.Circ rna‐0072309 knockdown induced opposite effects, but could not affect apoptosis.Overexpressed mi r‐665 in tumor tissues was targeted and negatively controlled by circ rna‐0072309.The pi3k/akt and wnt/β‐catenin pathways were inhibited by abundant circ rna‐0072309.Mi r‐665 overexpression disturbed those effects derived from pc‐circ.The circ rna‐0072309 had antitumor influences in hep3b cell line through targeting mi r‐665 relying on the deactivation of pi3k/akt and wnt/β‐catenin pathways.

Journal: Biofactors (2020)
Publication types: Research Article;
Effects of long noncoding RNA SPRY4-IT1-mediated EZH2 on the invasion and migration of lung adenocarcinoma

We aim to investigate the interaction between the ezh2 and the long noncoding rna (lnc rna) spry4‐it1.We also explore their respective effects on human lung adenocarcinoma (la) cell invasion and migration.Both la and adjacent normal tissues were obtained from 256 la patients.Spty4‐it expression and ezh2 m rna expressions in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction (rt‐q pcr).The si rnas against spry4‐it1 and ezh2 were co‐transfected into a549 and h1975 cells.The interaction between spry4‐it1 and ezh2 was determined using a rna pull‐down assay and a rna immunoprecipitation (rip) assay.A transwell assay and scratch assay were used to evaluate the cell migration and invasion abilities.The expressions of e‐cadherin and vimentin in the epithelial‐mesenchymal transition (emt) and ezh2 protein expression were detected through western blotting.Spry4‐it1 expression was observed to be significantly lower, while the expression of ezh2 was higher in the la tissues than in the adjacent normal tissues.Compared with the hbe cell line, expressions of spry4‐it1 in each human la cell line had decreased, with the lowest observed reduction in the a549 cell line, while ezh2 m rna and protein expression increased in each human la cell lines.After spry4‐it1‐si rna was transfected into a549 and h1975 cells, invasion and migration abilities were enhanced, in addition to a reduction in the expression of e‐cadherin, while expressions of vimentin exhibited an increased rate.Consequently, we find that ezh2 promotes la cell invasion and metastasis by inhibiting spry4‐it1 expression.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Effects of gene knockdown of CNP on ventricular remodeling after myocardial ischemia-reperfusion injury through NPRB/Cgmp signaling pathway in rats

This study aimed to explore effects of cnp on ventricular remodeling following myocardial ischemia‐reperfusion (i/r) injury through the nprb/c gmp signaling pathway.Rat cardiomyocytes were assigned into: control, i/r, i/r + cnp, and i/r + 8‐br‐c gmp groups.Elisa, q rt‐pcr, and western blotting were used to detect c gmp content and expression, respectively.After model establishment of i/r rats, normal control, cnp −/− control, i/r, and cnp −/− groups were set.Indexes of heart were detected using echocardiography and hemodynamics.Elisa was used to measure serum cnp, c gmp, ldh, c tn i, ck‐mb, tnf‐α, and il‐6 levels.Myocardial infarct was identified by ttc staining, and apoptosis conditions by tunel staining.Qrt‐pcr and western blotting were adopted to detect expressions of cnp, nprb, c gmp, and apoptosis‐related genes.Compared with control group, c gmp contents and expression in the i/r, i/r + cnp and i/r + 8‐br‐c gmp groups were decreased.Levels of lvedv, lvesv, lvds, lvdd, ivsd, lvm, lvedp, and lvsp were higher in the i/r, cnp −/− control, and cnp −/− groups than normal control group while lvef, sv, co, and ±dp/dtmax were lower.Compared with the normal control group, ldh, c tn i, ck‐mb, tnf‐α, and il‐6 were higher in the i/r, cnp −/− control and cnp −/− groups; pathological changes and myocardial infarction were observed in the i/r, cnp −/− control, and cnp −/− groups; expressions of apoptosis‐related genes in those groups were higher; while cnp, nprb, c gmp, and bcl‐2 expressions were decreased.We came to the conclusion that gene knockdown of cnp blocks the nprb/c gmp signaling pathway, thereby aggravating myocardial i/r injury and causing ventricular remodeling in rats.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Synergistic effect of siRNA-mediated silencing of TGF-β R1 and TGF-β R2 genes on the proliferation and apoptosis of penile urethral epithelial cells in hypospadiac male rats

The study elucidated the effects associated with silencing growth factor‐β r1 ( tgf‐β r1 ) and tgf‐β r2 genes on the proliferation and apoptosis of penile urethral epithelial cells (uecs) in hypospadiac male rats.Seventy‐five male rats were distributed into the normal, model, tgf‐β r1/2 ‐si rna, tgf‐β r1 ‐si rna and tgf‐β r2 ‐si rna groups.The uecs of the rats included in the study were cultured in vitro and subsequently divided into the control, blank, tgf‐β r1/2 ‐si rna, tgf‐β r1 ‐si rna and tgf‐β r2 ‐si rna groups.The m rna and protein expressions of tgf‐β r1 / r 2 were measured by quantitative real‐time polymerase chain reaction (q rt‐pcr) and western blotting.Cell proliferation and apoptosis were evaluated by cell counting kit‐8 (cck‐8) assay as well as by flow cytometry.Compared with the normal group, the apoptotic rate of the uecs in the model, tgf‐β r1/2 ‐si rna, tgf‐β r1 ‐si rna and tgf‐β r2 ‐si rna groups displayed remarkable increases; compared with the model group, the apoptotic rate of the uecs in the tgf‐β r1/2 ‐si rna, tgf‐β r1 ‐si rna and tgf‐β r2 ‐si rna groups displayed significant decreases, similar observations were made regarding m rna and protein expressions of tgf‐β r1 and tgf‐β r 2.Compared with the tgf‐β r1/2 ‐si rna group, the apoptotic rates of the uecs in the tgf‐β r1 ‐si rna and tgf‐β r2 ‐si rna groups were up regulated, while cell proliferation in the tgf‐β r1 ‐si rna and tgf‐β r2 ‐si rna groups decreased accompanied by an increased rate of apoptosis.This study ultimately demonstrated that the silencing of tgf‐β r1 and tgf‐β r2 genes could promote cell proliferation and inhibit apoptosis of penile uecs in hypospadiac male rats.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Genetic deletion of GIT2 prolongs functional recovery and suppresses chondrocyte differentiation in rats with rheumatoid arthritis

The current study was conducted for investigating the mechanism by which git2 gene deletion affects the functional recovery and chondrocyte differentiation in rats with rheumatoid arthritis (ra).Thirty‐two rats were randomly divided into normal, model, git2 gene knockout (git2‐ko), and model + git2‐ko groups.Hematoxylin‐eosin (he) staining was performed for the observation of synovial tissues.Immunohistochemistry examinations were conducted to determine type ii collagen expression as well as identify chondrocyte differentiation.Q rt‐pcr and western blotting techniques were adopted in order to expressions of interleukin‐1β (1l‐1β), tumor necrosis factor‐α (tnf‐α), aggrecan, and sry‐related hmg box 9 (sox9).A tape measure and vernier caliper were used to measure the degree of swelling.Compared with synovial tissues in the model group, those in the model + git2‐ko group, were thicker and comprised of a mass of inflammatory cells ( p &lt; 0.05).Compared with the model group, the type ii collagen expressions of the cartilage tissues of the rats decreased in the model + git2‐ko group ( p &lt; 0.05).In terms of the degree of swelling in cartilage tissues, the model group displayed a lesser degree of swelling than in that of the model + git2‐ko group ( p &lt; 0.05).When compared with the model + git2‐ko group, the m rna expressions of 1l‐1β, tnf‐α, aggrecan, sox9 and the relevant protein expressions were lower in the model group (all p &lt; 0.05).Git2 gene deletion might weaken chondrocyte differentiation in rats with ra, as a result acting to ultimately prolong the functional recovery of ra.

Journal: Journal of Cellular Biochemistry (2017)
Publication types: Research Article;
Down-regulation of microRNA let-7d inhibits the proliferation and invasion of trophoblast cells in preeclampsia

Preeclampsia (pe) is a serious pregnancy complication that continues to adverse effects on mother and the fetus.The study investigated the effect of micro rna let‐7d (mi r‐let‐7d) on the proliferation and invasion of trophoblast cells (tc) in pe.In situ hybridization techniques were employed to evaluate the mi r‐let‐7d expressions in the placental tissues from 63 pe patients as well as 65 normal placental tissues.Transfection of pre‐let‐7d, anti‐let‐7d, and their corresponding control sequences was performed in tcs obtained from pe.The blank group was composed of tcs no transfection and normal group consisted of normal tcs.Expressions of proliferation and invasion markers in tcs were detected by q rt‐pcr.Proliferation, apoptosis, and the invasion ability of the tcs were determined using a cck‐8 assay, flow cytometry, and transwell assay.In comparison to the normal placental tissues, pe placental tissues exhibited increased levels of let‐7d expression.Following transfection of anti‐let‐7d, when compared with the blank group, the anti‐let‐7d group displayed increased levels of proliferation ability, expression of proliferation labeling proteins pcna and ki67, number of tcs as well as expressions of the invasion related proteins mmp‐2, mmp‐9, and timp‐1.In contrast declines in cell apoptosis rate were observed.Compared with the blank group, the changes of the indexes were reversed in the pre‐let‐7d group.The study provided evidence suggesting that low expression levels of mi r‐let‐7d plays a central role in suppressing apoptosis in addition to promoting the proliferation and invasion of pe tcs.

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