syedzayyan/paper_mill_benchmark huggingface dataset:
Downregulated long noncoding RNA LINC00313 inhibits the epithelial-mesenchymal transition, invasion, and migration of thyroid cancer cells through inhibiting the methylation of ALX4

Thyroid cancer represents one of the prevalent endocrine cancer with relatively high incidence rate around the world, accompanied by unchanged fatality rate.We probe into the specific role of linc00313 in mediation of cellular processes of thyroid cancer including proliferation, migration, and invasion through the methylation of aristaless‐like homeobox 4 (alx4).Thyroid cancer‐related long noncoding rnas (lnc rnas) and genes were analyzed by microarray‐based analysis.The antitumor effect of linc00313 was examined with the gain‐ and loss‐of‐function experiments.In addition, the binding of linc00313 and the promoter region of alx4, and the interaction of linc00313 with methylation‐related proteins were detected.Later, xenograft tumors in nude mice were induced expecting to dig out the modulatory function of linc00313 in tumor growth of thyroid carcinoma.The microarray‐based analysis manifested that linc00313 was overexpressed, whereas alx4 was downregulated in thyroid cancer, the results of which were also verified in thyroid cancer tissues.Besides, our results demonstrated that linc00313 bound to the alx4 promoter region, and linc00313 recruited dnmt1 and dnmt3b proteins to promote the methylation of alx4 promoter region, thus suppressing the alx4 expression.Finally, the downregulation of linc00313 and upregulation of alx4 repressed the akt/m tor signaling axis, thus inhibiting proliferative, migratory, invasive abilities as well as epithelial‐to‐mesenchymal transition (emt) of thyroid cancer cells.Collectively, downregulated linc00313 suppresses cell proliferation, migration, as well as invasion of thyroid cancer by inhibiting the methylation of alx4 and increasing its expression by inactivation of the akt/m tor signaling pathway.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
Long noncoding RNA nuclear enriched abundant transcript 1 impacts cell proliferation, invasion, and migration of glioma through regulating miR-139-5p/ CDK6

Aims : we aimed to explore the impact of long noncoding rna (lnc rna) nuclear enriched abundant transcript 1 (neat1) on cell proliferation, invasion, and migration of glioma.Methods : differentially expressed genes were screened out from gene expression omnibus data set based on the microarray analysis.The expression levels of lnc rna neat1, mi r‐139‐5p, and cdk6 in glioma cells and tissues were examined by quantitative reverse transcription polymerase chain reaction, and the protein level of cdk6 in glioma cells was determined by western blot and immunohistochemistry.Glioma cell viability, cell cycle, and apoptosis were detected by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazoliumbromide (mtt) and flow cytometry, respectively, whereas cell invasion and migration were analyzed by transwell assay.The target relationships among neat1, mi r‐139‐5p, and cdk6 were confirmed by dual‐luciferase reporter gene assay.The effects of lnc rna neat1 on tumor growth were further testified through glioma xenografts in nude mice.Results : lnc rna neat1 and cdk6 were highly expressed in glioma tissues and cells, whereas mi r‐139‐5p was lowly expressed.There were target relationships and correlations on expressions between mi r‐139‐5p and neat1/ cdk6.Neat1 and cdk6 could promote cell proliferation and metastasis of glioma cells and impeded cell apoptosis, whereas mi r‐139‐5p exerted suppressive effects on the biological functions of glioma cells.Neat1 regulated cdk6 to affect glioma growth through sponging mi r‐139‐5p.Conclusions : lnc rna neat1 promotes cell proliferation, invasion, and migration of glioma through regulating mi r‐139‐5p/cdk6 pathway.

Journal: Journal of Cellular Physiology (2018)
Publication types: Research Article;
MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

The aim of the present study was to explore the mechanism through which mi r-130a-3p affects the viability, proliferation, migration, and invasion of nasopharyngeal carcinoma (npc).Tissue samples were collected from the hospital department.Npc cell lines were purchased to conduct the in vitro and in vivo assays.A series of biological assays including mtt, transwell, and wound healing assays were conducted to investigate the effects of mi r-130a-3p and bach2 on npc cells.Mi r-130a-3p was down-regulated in both npc tissues and cell lines, whereas bach2 was up-regulated in both tissues and cell lines.Mi r-130a-3p overexpression inhibited npc cell viability, proliferation, migration, and invasion but promoted cell apoptosis.The converse was true of bach2, the down-regulation of which could inhibit the corresponding cell abilities and promote apoptosis of npc cells.The target relationship between mi r-130a-3p and bach2 was confirmed.The epithelial–mesenchymal transition (emt) pathway was also influenced by mi r-130a-3p down-regulation.In conclusion, mi r-130a-3p could bind to bach2, inhibit npc cell abilities, and promote cell apoptosis.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

It has been reported that mi r-486-3p expression is decreased in retinoblastoma (rb) tumor tissues, however, its function in rb has been less reported.The present study aimed to explore the regulatory effects of mi r-486-3p on rb cells.The expression of mi r-486-3p in rb tissues and cells was detected by quantitative real-time polymerase chain reaction (q rt-pcr).Cell viability, proliferation, apoptosis, migration and invasion ability were determined by cell counting kit-8 (cck-8) kit, clone formation assay, flow cytometry, scratch assay and transwell, respectively.Targetscan 7.2 and dual-luciferase reporter were used to verify target genes for mi r-486-3p.The expressions of apoptosis-related proteins and ecm1 were detected by western blot.The mi r-486-3p expression was decreased in rb tissues and cells.In rb cells, overexpression of mi r-486-3p inhibited cell proliferation, migration and invasion, while promoted apoptosis.Moreover, overexpression of mi r-486-3p decreased bcl-2 expression, while increased the expressions of bax and cleaved caspase-3 (c caspase-3).Ecm1 was the target gene of mi r-486-3p, and mi r-486-3p inhibited the expression of ecm1.Furthermore, ecm1 partially reversed the inhibitory effect of mi r-486-3p on the proliferation, migration and invasion of rb cells.Mi r-486-3p inhibited the proliferation, migration and invasion of rb by down-regulating ecm1.

Journal: Bioscience Reports (2020)
Publication types: Research Article;
MiR-942 regulates the function of breast cancer cell by targeting FOXA2

Micro rna (mi r)-942 regulates the development of a variety of tumors, however, its function in breast cancer (bca) has been less reported.Therefore, the present study investigated the regulatory effects of mi r-942 on bca cells.The expression of mi r-942 in whole blood samples and bca cell lines was detected by quantitative real-time (q rt)-pcr.Direct target gene for mi r-942 was confirmed by dual-luciferase reporter assay.Foxa2 expression in adjacent tissues was detected by q rt-pcr.The effects of mi r-942, or mi r-942 with foxa2, on the cell viability, proliferation, apoptosis, migration and invasion of bca cells were determined by cell counting kit-8 (cck-8), colony formation assay, flow cytometry, wound scratch and transwell, respectively.The levels of n-cadherin, e-cadherin and snail were determined by western blot.Kaplan–meier was used to explore the relationship among the expressions of mi r-942 and foxa2 and the prognosis of bca patients.Mi r-942 had high expressed in bca, while its low expression significantly suppressed the cell viability, proliferation, migration and invasion of bca, but increased cell apoptosis.Down-regulation of n-cadherin and snail and up-regulation of e-cadherin were also induced by low-expression of mi r-942.Foxa2, which was proved as the direct target gene for mi r-942 and was low-expressed in bca, partially reversed the effect of overexpressed mi r-942 on promoting cell viability, proliferation, migration and invasion, and suppressed cell apoptosis.A lower survival rate was observed in bca patients with a high expression of mi r-942 and a low expression of foxa2.Mi r-942 promoted the progression of bca by down-regulating the expression of foxa2.

Journal: Bioscience Reports (2019)
Publication types: Research Article;
Long noncoding RNA HOXA-AS2 promotes non-small cell lung cancer progression by regulating miR-520a-3p

Background: the hoxa cluster antisense rna 2 (hoxa-as2) has recently been discovered to be involved in carcinogenesis in multiple cancers.However, the role and underlying mechanism of hoxa-as2 in non-small cell lung cancer (nsclc) yet need to be unraveled.Methods: hoxa-as2 expression in nsclc tissues and cell lines was detected using quantitative real-time pcr (q rt-pcr).Furthermore, the effects of hoxa-as2 on nsclc cell proliferation, apoptosis, migration, and invasion were assessed by mts, flow cytometry, wound healing and transwell invasion assays, respectively.Starbase2.0 predicted and luciferase reporter and rna immunoprecipitation (rip) assays were used to validate the association of hoxa-as2 and mi r-520a-3p in nsclc cells.Results: our results revealed that hoxa-as2 in nsclc tissues were up-regulated and cell lines, and were associated with poor prognosis and overall survival.Further functional assays demonstrated that hoxa-as2 knockdown significantly inhibited nsclc cell proliferation, induced cell apoptosis and suppressed migration and invasion.Starbase2.0 predicted that hoxa-as2 sponge mi r-520a-3p at 3′-utr, which was confirmed using luciferase reporter and rip assays.Mi r-520a-3p expression was inversely correlated with hoxa-as2 expression in nsclc tissues.In addition, mi r-520a-3p inhibitor attenuated the inhibitory effect of hoxd-as2-depletion on cell proliferation, migration and invasion of nsclc cells.Moreover, hoxa-as2 could regulate hoxd8 and map3k2 expression, two known targets of mi r-520a-3p in nsclc.Conclusion: these findings implied that hoxa-as2 promoted nsclc progression by regulating mi r-520a-3p, suggesting that hoxa-as2 could serve as a therapeutic target for nsclc.

Journal: Bioscience Reports (2019)
Publication types: Research Article;
Circ_002117 binds to microRNA-370 and promotes endoplasmic reticulum stress-induced apoptosis in gastric cancer

Background mounting evidence implicates circular rnas (circ rnas) in various biological processes during cancer progression.Gastric cancer is a main cause of cancer-related deaths worldwide.Herein, we aimed at investigating whether circ_002117 mediates gastric cancer progression through endoplasmic reticulum (er) stress.Methods bioinformatics analysis detected differentially expressed circ rnas and their target mi rna candidates, and rt-q pcr was performed to detect expression of circ_002117, micro rna (mi rna)-370 and herpud1 in gastric cancer tissues and cells.Gastric cancer cells were transfected with plasmids and their proliferative ability and apoptosis were detected with gain- and loss-of-function assay.The er of treated cells was observed under a transmission electron microscope.Dual-luciferase reporter gene assay and rip were performed to detect the interaction between heprud1, mi r-370 and circ_002117-treated cells were injected into mice to establish xenograft tumor model.Results circ_002117 and heprud1 were poorly expressed whereas mi r-370 was highly expressed in clinical cancer tissues and cells.Circ_002117 was indicated to target and suppress mi r-370 expression, while herpud1 was directly targeted by mi r-370.Circ_002117 overexpression or mi r-370 deficiency promoted er stress-induced apoptosis and decreased proliferation of gastric cancer cells, which was reversed by silencing of heprud1.Circ_002117 overexpression or mi r-370 depletion significantly suppressed gastric cancer tumorigenesis in vivo .Conclusions taken altogether, circ_002117 facilitated er stress-induced apoptosis in gastric cancer by upregulating herpud1 through mi r-370 inhibition.

Journal: Cancer Cell International (2020)
Publication types: Research Article;
Association of cord blood asprosin concentration with atherogenic lipid profile and anthropometric indices

Background elevated lipids in umbilical cord blood affect fetal programming, leading to a higher risk of developing cardiovascular disease in later life.However, the causes of changes in the lipid profile of umbilical cord blood are not clear yet.This study aimed for the first time to determine the association of asprosin concentration with tag, tc, hdl-c, ldl-c concentrations and tag/hdl-c, tc/hdl-c, ldl-c/hdl-c and non-hdl-c/hdl-c ratio in umbilical cord blood as well as newborn anthropometric indices.This cross-sectional study was based on 450 mother- newborn pairs of a birth cohort study in sabzevar, iran.Multiple linear regression was used to estimate the association of lipid concentration and lipid ratios as well as birth weight (bw), birth length (bl), head circumference (hc) and chest circumference (cc) with asprosin in cord blood samples controlled for the relevant covariates.Result in fully adjusted models, each 1 ng/m l increase in asprosin was associated with 0.19 (95% ci 0.06, 0.31, p &lt; 0.01), 0.19 (95% ci 0.10, 0.29, p &lt; 0.01), 0.17 (95% ci 0.09, 0.25, p &lt; 0.01), 0.17 (95% ci 0.09, 0.25, p &lt; 0.01), 0.01 (95% ci 0.00, 0.013, p &lt; 0.01), 0.01 (95% ci 0.01, 0.01, p &lt; 0.01), 0.01 (95% ci 0.01, 0.01, p &lt; 0.01) and 0.01 (95% ci 0.01, 0.01, p &lt; 0.01) increase in tag, tc, ldl-c, tag/hdl-c, tc/hdl-c, ldl-c/hdl-c and non-hdl-c/hdl-c ratio respectively.Moreover, higher asprosin levels was positively associated with newborn bw, bl, hc and cc; however, these associations were not statistically significant.Conclusion overall, our findings support the positive association between cord asprosin concentration and the development of atherogenic lipid profile in newborns.Further studies are needed to confirm the findings of this study in other populations.

Journal: Diabetology & Metabolic Syndrome (2022)
Publication types: Research Article;
Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma

Glioma is the most prevalent solid tumor in the central nervous system (cns).Recently, it has been indicated that long non-coding rnas (lnc rnas) substantially adjust the development of a variety of human cancers.In the present study, it was found and verified via microarray analysis that lnc rna psma3-as1 exhibited a high expression in glioma tissues and cell lines.Then cck-8, 5-ethynyl-2′-deoxyuridine (ed u) staining, plate clone assay, transwell assay, western blotting and nude mouse model were adopted to verify psma3-as1’s effects on glioma.Knockdown of psma3-as1 inhibited the migration, proliferation and invasion of glioma cells in vivo and in vitro.Besides, psma3-as1 bound to mi r-302a-3p directly reduced the expression of mi r-302a-3p, thus functioning as an endogenous sponge confirmed by luciferase reporter assay and bioinformatics analysis.Psma3-as1 knockdown remarkably enhanced the role of mi r-302a-3p overexpression in cell behaviors in glioma.Moreover, these assays also confirmed that rab22a was a target of mi r-302a-3p.In this research, therefore, the psma3-as1/mi r-302a-3p/rab22a pathway regulatory axis may be revealed in the pathogenesis of glioma, and psma3-as1 can be used as an underlying target for the treatment and prognosis of glioma.

Journal: Bioscience Reports (2020)
Publication types: Research Article;
MicroRNA-802 inhibits epithelial-mesenchymal transition through targeting Flotillin-2 in human prostate cancer

Mi rnas are a class of non-coding rnas that exert critical roles in various biological processes.The aim of the present study was to identify the functional roles of mi r-802 in regulating epithelial–mesenchymal transition (emt) in prostate cancer (pca).Mi r-802 expression was detected in 73 pairs of pca samples and pca cell lines (pc3 and du145 cells) by q rt-pcr.Cell proliferation was detected using mtt assay, and cell apoptosis was evaluated using flow cytometry.Transwell assay was conducted to investigate cell migration and invasion.Expression analysis of a set of emt markers was performed to explore whether mi r-802 is involved in emt program.Xenograft model was established to investigate the function of mi r-802 in carcinogenesis in vivo.The direct regulation of flotillin-2 (flot2) by mi r-802 was identified using luciferase reporter assay.Mi r-802 was remarkably down-regulated in pca tissues and cell lines.Gain-of-function trails showed that mi r-802 serves as an ‘oncosuppressor’ in pca through inhibiting cell proliferation and promoting cell apoptosis in vitro.Overexpression of mi r-802 significantly suppressed in vivo pca tumor growth.Luciferase reporter analysis identified flot2 as a direct target of mi r-802 in pca cells.Overexpressed mi r-802 significantly suppressed emt, migration and invasion in pca cells by regulating flot2.We identified mi r-802 as a novel tumor suppressor in pca progression and elucidated a novel mechanism of the mi r-802/flot2 axis in the regulation of emt, which may be a potential therapeutic target.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
Long non-coding RNA PTPRG-AS1 promotes cell tumorigenicity in epithelial ovarian cancer by decoying microRNA-545-3p and consequently enhancing HDAC4 expression

Background long non-coding rna ptprg antisense rna 1 (ptprg-as1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development.Few reports have focused on the detailed role of ptprg-as1 in epithelial ovarian cancer (eoc) and its underlying mechanism.This study aimed to determine the physiological function of ptprg-as1 in eoc.A series of experiments were also performed to identify the mechanisms through which ptprg-as1 exerts its function in eoc.Methods reverse transcription-quantitative polymerase chain reaction was used to determine ptprg-as1 expression in eoc tissues and cell lines.Ptprg-as1 was silenced in eoc cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo.The putative mi rnas that target ptprg-as1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and rna immunoprecipitation assays.Results our data verified the upregulation of ptprg-as1 in eoc tissues and cell lines.High ptprg-as1 expression was associated with shorter overall survival in patients with eoc.Functionally, eoc cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by ptprg-as1 silencing.In contrast, cell apoptosis was promoted by loss of ptprg-as1.Regarding the mechanism, ptprg-as1 could serve as a competing endogenous rna in eoc cells by decoying micro rna-545-3p (mi r-545-3p), thereby elevating histone deacetylase 4 (hdac4) expression.Furthermore, rescue experiments revealed that ptprg-as1 knockdown-mediated effects on eoc cells were, in part, counteracted by the inhibition of mi r-545-3p or restoration of hdac4.Conclusions ptprg-as1 functioned as an oncogenic lnc rna that aggravated the malignancy of eoc through the mi r-545-3p/hdac4 ce rna network.Thus, targeting the ptprg-as1/mi r-545-3p/hdac4 pathway may be a novel strategy for eoc anticancer therapy.

Journal: Journal of Ovarian Research (2020)
Publication types: Research Article;
MicroRNA-320a acts as a tumor suppressor by targeting BCR/ABL oncogene in chronic myeloid leukemia

Accumulating evidences demonstrated that the induction of epithelial-mesenchymal transition (emt) and aberrant expression of micro rnas (mi rnas) are associated with tumorigenesis, tumor progression, metastasis and relapse in cancers, including chronic myeloid leukemia (cml).We found that mi r-320a expression was reduced in k562 and in cml cancer stem cells.Moreover, we found that mi r-320a inhibited k562 cell migration, invasion, proliferation and promoted apoptosis by targeting bcr/abl oncogene.As an upstream regulator of bcr/abl, mi r-320a directly targets bcr/abl.The enhanced expression of mi r-320a inhibited the phosphorylation of pi3k, akt and nf-κb; however, the expression of phosphorylated pi3k, akt and nf-κb were restored by the overexpression of bcr/abl.In k562, infected with mi r-320a or transfected with si bcr/abl, the protein levels of fibronectin, vimentin and n-cadherin were decreased, but the expression of e-cadherin was increased.The expression of mesenchymal markers in mi r-320a-expressing cells was restored to normal levels by the restoration of bcr/abl expression.Generally speaking, mi r-320a acts as a novel tumor suppressor gene in cml and mi r-320a can decrease migratory, invasive, proliferative and apoptotic behaviors, as well as cml emt, by attenuating the expression of bcr/abl oncogene.

Journal: Scientific Reports (2015)
Publication types: Research Article;
The profile of the key pro-inflammatory cytokines in the serum of patients with CD and their association with the disease severity and activity

Background the epidemiology of crohn’s disease (cd) has changed over the past decades, demonstrating a trend toward increased prevalence in developing countries, while in developed countries, its incidence has stabilized.The study aimed to examine the profile of the key pro-inflammatory cytokines in the serum of patients with cd and establish their association with the severity and activity of the disease.Methods a total of 61 patients (29 women (47.5%), 32 men (52.5%) aged from 18 to 40 years (mean age (30.42 ± 2.51) years) with the verified diagnosis of cd in the active phase were examined.The control group consisted of 30 healthy people of corresponding age.Results cd is characterized by a reliable increase of pro-inflammatory cytokines in blood compared to healthy people: tumor necrosis factor-α (tnf-α) – by 4.45 times (137.46 ± 9.72 vs.30.88 ± 2.08 pg/ml in healthy people, p &lt; 0,001), interleukin-1α (il-1α) – by 5.08 times (51.55 ± 4.36 vs.10.14 ± 0.93 pg/ml, p &lt; 0.001), interleukin-6 (il-6) – by 2.16 times (20.03 ± 1.81 vs.9.27 ± 0.52 pg/ml, p &lt; 0.001), interleukin-8 (il-8) – by 2.04 times (25.74 ± 2.05 vs.12.62 ± 1.16 pg/ml, p &lt; 0.001), and interferon-γ (ifn-γ) – by 5.30 times (208.63 ± 14.29 vs.39.35 ± 2.40 pg/ml, p &lt; 0.001).The authors have established direct correlations between the crohn's disease activity index and blood content of tnf-α ( r = 0.84, p &lt; 0.013), inf-γ ( r = 0.61, p &lt; 0.028); between tnf-α and inf-γ content ( r = 0.67, p &lt; 0.023), il-1α ( r = 0.49, p &lt; 0.042), il-6 ( r = 0.40, p &lt; 0.045), and il-8 ( r = 0.51, p &lt; 0.033); inf-γ and il-1α ( r = 0.53, p &lt; 0.040), il-6 ( r = 0.37, p &lt; 0.039), il-8 ( r = 0.44, p &lt; 0.040).Conclusions patients with cd were found to have multiple cytokines (tnf-α, il-1α, il-6, il-8, and ifn-γ,).The content of cytokines correlated positively with the cd activity index.

Journal: BMC Gastroenterology (2022)
Publication types: Research Article;