syedzayyan/paper_mill_benchmark huggingface dataset:
Interferon characterization associates with asthma and is a potential biomarker of predictive diagnosis

Interferon (ifn) plays a role in immune and inflammation responses.However, the effect of ifn in asthma is still not fully clear.The present study was conducted to better understand the role of ifn signatures in asthma.Blood samples from case–control studies (study 1: 348 asthmas and 39 normal controls and validation study 2: 411 asthmas and 87 normal controls) were enrolled.The single-sample gene set enrichment analysis (ss gsea) method was used to quantify the levels of 74 ifn signatures.Gene ontology analysis and pathway function analysis were performed for functional analysis and a protein–protein interaction (ppi) network was constructed.The area under the curve (auc) value was used to evaluate the diagnostic ability.In our work, ifn-γ response-dn, negative regulation of ifn-γ secretion, ifng pathway, negative regulation of response to ifn-γ, and type 1 ifn biosynthetic process showed higher levels in asthma.Functional analysis demonstrated that pathway and biological process involved in ifn signaling pathway, regulation of type 1 ifn production and response to ifn-γ.Hub ifn-related genes were identified, and their combination as biomarker exhibited a good diagnostic capacity for asthma (auc = 0.832).These findings offered more insight into the underlying mechanism of how ifn signatures affected asthma.The use of the easy-to-apply ifn-related genes might serve as a promising blood-based biomarker for early diagnosis of asthma.

Journal: Bioscience Reports (2021)
Publication types: Research Article;
MicroRNA‐222 promotes tumorigenesis via targeting DKK2 and activating the Wnt/β‐catenin signaling pathway

Mi r‐222 in glioma can regulate cell cycle progression and apoptosis.However, the relationship between mi r‐222 and wnt/β‐catenin signaling pathway in glioma remains unknown.Here, we found that the dickkopf‐2 gene ( dkk2 ) was a direct target of mi r‐222 by target prediction analysis and dual luciferase reporter assay.Rna interference silencing of dkk2 proved that mi r‐222 overexpression led to constitutive activation of β‐catenin through inhibition of dkk2 expression in glioma cells.Furthermore, mi r‐222 si rna significantly inhibited tumorigenesis in vivo.Finally, western blot analysis showed that mi r‐222 could regulate the expression of β‐catenin and the downstream genes of wnt/β‐catenin signaling pathway.Taken together, our findings reveal a new regulatory mechanism of mi r‐222 and suggest that mi r‐222 might be a potential target in glioma therapy.

Journal: FEBS Letters (2013)
Publication types: Research Article;
Effects of microRNA-374 on proliferation, migration, invasion, and apoptosis of human SCC cells by targeting Gadd45a through P53 signaling pathway

The present study investigated the effects of micro rna-374 (mi r-374) on human squamous cell carcinoma (scc) cell proliferation, migration, invasion, and apoptosis through p53 signaling pathway by targeting growth arrest and dna-damage-inducible protein 45 α (gadd45a).Skin samples were collected from patients with skin scc and normal skin samples.Expression of mi r-374, gadd45a, p53, p73, p16, c-myc, bcl-2, bax, caspase-3, and caspase-9 were detected using quantitative real-time polymerase chain reaction (q rt-pcr) and western blotting.A431 and scl-1 cells were divided into blank, negative control (nc), mi r-374 mimics, mi r374 inhibitors, si rna–gadd45a, and mi r-374 inhibitors + si rna–gadd45a groups.Their proliferation, migration, invasion, cell cycle, and apoptosis were evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (mtt) assay, scratch test, transwell assay, and flow cytometry.Scc skin tissues exhibited decreased expression of mi r-374, p73, p16, bax caspase-3 and caspase-9, and increased levels of gadd45a, p53, c-myc, and bcl-2 compared with the normal skin tissues.The mi r-374 inhibitors group exhibited decreased expression of mi r-374, p73, p16, bax caspase-3 and caspase-9, and increased expression of gadd45a, p53, c-myc, and bcl-2, enhanced cell proliferation, migration, and invasion, and reduced apoptosis compared with the blank and nc groups; the mi r-374 mimics group followed opposite trends.Compared with the blank and nc groups, the mi r-374 inhibitors + si rna–gadd45a group showed decreased mi r-374 level; the si rna–gadd45a group showed elevated levels of p73, p16, bax, caspase-3 and caspase-9, decreased levels of gadd45a, p53, c-myc, and bcl-2, reduced cell proliferation, migration, and invasion, and accelerated apoptosis.Mi r-374 induces apoptosis and inhibits proliferation, migration, and invasion of scc cells through p53 signaling pathway by down-regulating gadd45a.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
Effects of microRNA-136 on melanoma cell proliferation, apoptosis, and epithelial–mesenchymal transition by targeting PMEL through the Wnt signaling pathway

The study aims to evaluate the effects of mi r-136 on the proliferation, apoptosis, and epithelial–mesenchymal transition (emt) of melanoma cells by targetting premelanosome protein (pmel) through the wnt signaling pathway.After establishment of melanoma mouse models, melanoma (model group) and normal tissues (normal group) were collected.Immunohistochemistry was performed to determine pmel protein concentration.Mouse melanoma cells were assigned into control, blank, negative control (nc), mi r-136 mimics, mi r-136 inhibitors, si rna-pmel, and mi r-136 inhibitors + si rna-pmel, li c1 (wnt signaling pathway activator), and si rna-pmel+ li cl groups.Mtt, scratch test, transwell assay, and flow cytometry were performed to measure cell proliferation, migration, invasion, and apoptosis.Quantitative real-time pcr (q rt-pcr) and western blotting were performed to evaluate mi r-136, pmel, β-catenin, wnt3a, bcl-2, bax, caspase, e-cadherin, and n-cadherin expressions.Pmel is highly expressed in melanoma tissues.Mi r-136, bax, caspase, and e-cadherin expressions decreased in the model group, whereas pmel, β-catenin, bcl-2, wnt3a, and n-cadherin expressions increased.Bax, caspase, and e-cadherin expressions increased in the mi r-136 mimics and si rna-pmel groups, whereas the expressions decreased in the mi r-136 inhibitors group and li c1 group.Pmel, β-catenin, bcl-2, wnt3a, and n-cadherin expressions, cell proliferation, migration, and invasion decreased, and the apoptosis rate inceased in the mi r-136 mimics and si rna-pmel groups; whereas the tendencies were opposite to those in the mi r-136 inhibitors group and li c1 group.In the si rna-pmel+ li cl group, pmel expression decreased.These findings indicated that overexpression of mi r-136 inhibits melanoma cell emt, proliferation, migration, invasion, and promotes apoptosis by targetting pmel through down-regulation of the wnt signaling pathway.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
MicroRNA-379 inhibits the proliferation, migration and invasion of human osteosarcoma cells by targeting EIF4G2

Osteosarcoma (os) is an aggressive malignant mesenchymal neoplasm amongst adolescents.The aim of the present study was to explore the various modes of action that mi r-379 has on the proliferation, migration, and invasion of human os cells.Mi r-379 achieves this by targetting eukaryotic initiation factor 4gii (eif4g2).Human os cell lines u2os and mg-63 were selected and assigned into blank, mi r-379 mimics, mi r-379 mimic negative control (nc), mi r-379 inhibitors, mi r-379 inhibitor nc, eif4g2 sh rna, control sh rna, and mi r-379 inhibitor + eif4g2 sh rna group.The mi r-379 expression and eif4g2 m rna expression were detected utilising quantitative real-time pcr (q rt-pcr) and the eif4g2 protein expression using western blotting.Mtt assay, scratch test, transwell assay, and flow cytometry were performed to determine the proliferation, migration, invasion, and cell cycle, respectively.In comparison with the mi r-379 mimic nc group, the mi r-379 mimics group had decreased eif4g2 expression; the mi r-379 inhibitors group indicated an increased eif4g2 expression.Compared with the control sh rna group, the eif4g2 expression was lower in the eif4g2 sh rna group and the mi r-379 expression was dropped in the mi r-379 inhibitor + eif4g2 sh rna group.The proliferation, migration, and invasion abilities of os cells were reduced in the mi r-379 mimics and eif4g2 sh rna groups.The percentage of os cells at the g0/g1 stage was increased, and the percentage at the s-stage was decreased in the mi r-379 mimics and eif4g2 sh rna groups.Mi r-379 may inhibit the proliferation, migration and invasion of os cells through the down-regulation of eif4g2.

Journal: Bioscience Reports (2017)
Publication types: Research Article;
lncRNA TINCR sponges miR-214-5p to upregulate ROCK1 in hepatocellular carcinoma

Background our preliminary bioinformatics analysis showed that lnc rna tincr may absorb mi r-214-5p by serving is sponge, while mi r-214-5p targets rock1.This study aimed to investigate the interactions among these 3 factors in hepatocellular carcinoma (hcc).Methods expression of tincr, rock1 and mi r-214-5p in hcc and non-tumor tissues was detected by performing q pcr.The correlations among tincr, rock1 and mi r-214-5p in hcc tissues were analyzed by performing linear regression.Overexpression experiments were performed to analyze gene interactions.Cell proliferation was analyzed by cck-8 assay.Results we found that tincr and rock1 were upregulated, while mi r-214-5p was downregulated in hcc.Tincr and rock1 were positively correlated, while tincr and mi r-214-5p were not significantly correlated.In hcc cells, tincr overexpression is followed by rock1 overexpression, while mi r-214-5p overexpression induced the downregulation of rock1.In addition, tincr and mi r-214-5p did not affect the expression of each other.Tincr and rock1 overexpression led to increased rate of cancer cell proliferation, while mi r-214-5p played an opposite role and reduced the effects of tincr overexpression.Therefore, tincr sponges mi r-214-5p to upregulate rock1 in hcc, thereby promoting cancer cell invasion and migration.

Journal: BMC Medical Genetics (2020)
Publication types: Research Article;
MicroRNA-27a Promotes the Proliferation and Invasiveness of Colon Cancer Cells by Targeting SFRP1 through the Wnt/β-Catenin Signaling Pathway

This study aims to explore the effects of micro rna-27a (mi r-27a) on the proliferation and invasiveness of colon cancer cells through the secreted frizzled-related protein 1 (sfrp1) and the wnt/β-catenin signaling pathway.Methods: colon cancer tissues and adjacent normal tissues from 125 colon cancer patients, together with the hcepic, hct-116, ht-29, sw480 and sw620 cell lines, were prepared for this study.The transfected hct-116 cells were divided into the mi r-27a mimics, mi r-27a-nc, anti-mi r-27a, blank, lv-sfrp1, lv-nc, and mi r-27a mimics + lv-sfrp1 groups.Rt-q pcr was performed to detect the expressions of mi r-27a and sfrp1 m rna.A dual-luciferase reporter assay was conducted to examine the effect of mi r-27a on sfrp1.Western blotting was used to measure the expressions of the sfrp1, β-catenin, gsk-3β, p-β-catenin, p-gsk-3β, c-myc and cyclin d1 proteins.Mtt, soft agar clone formation and transwell chamber assays were performed to detect cell proliferation and invasion.Results: compared with normal tissues and cells, colon cancer tissues and cells demonstrated significantly higher expression of mi r-27a, but lower expressions of sfrp1 m rna and protein.Mi r-27a negatively regulated the expression of sfrp1 m rna.Sfrp1 was also found to be a target gene of mi r-27a.In the mi r-27a mimic group, the proliferation and invasiveness of colon cancer cells were significantly increased, while the expressions of gsk-3 β and p-β-catenin were remarkably down-regulated; in contrast, the expressions of p-gsk-3β, -catenin, c-myc and cyclin d1 were up-regulated.While the proliferation and invasiveness of colon cancer cells in the anti-mi r-27a and lv-sfrp1 groups were decreased, the expressions of gsk-3β and p-β-catenin were elevated, and the expressions of p-gsk-3β, β-catenin, c-myc and cyclin d1 were decreased.Conclusion: these findings indicated that mi r-27a could promote the proliferation and invasiveness of colon cancer cells by targeting sfrp1 through the wnt/β-catenin signaling pathway.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
MicroRNA-200a Affects the Proliferation of Airway Smooth Muscle Cells and Airway Remodeling by Targeting FOXC1 via the PI3K/AKT Signaling Pathway in Ovalbumin-Induced Asthmatic Mice

The etiology of asthma, which is a complicated disorder with various symptoms, including wheezing, coughing, and airflow obstruction, remains poorly understood.In addition, the effects of micro rnas (mi rs) have not been explored.This study explored the effect of micro rna-200a (mi r-200a) on airway smooth muscle cells (asmcs) and airway remodeling in asthmatic mice.Furthermore, we speculated that mi r-200a achieves its effect by targeting foxc1 via the pi3k/akt signaling pathway based on differentially expressed gene screening, target mi r predictions and a bioinformatics analysis.Methods: eighty mice were assigned to a saline group or an ovalbumin (ova) group, and the ova group was transfected with a series of inhibitors, activators, and si rnas to test the established mouse model.Airway reactivity and the ratio of eosinophils (eoss) to leukocytes were detected.An elisa was adopted to measure the levels of interleukin (il)-4, il-6, il-8, tumor necrosis factor (tnf)-α, and immunoglobulin e (ig e).Reverse transcription quantitative polymerase chain reaction (rt-q pcr) and western blotting were used to determine the expression of foxc1, pi3k, akt, nf-κb, cyclin d1, tgf-β1 and p-akt in asmcs.Finally, cck-8 assays were performed to detect cell proliferation and flow cytometry to detect apoptosis and cell cycle entry.Results: the bioinformatics analysis indicated that mi r-200a mediated the pi3k/akt signaling pathway by targeting foxc1.In addition, mouse models of asthma were established.An elevated expression of mi r-200a, a decreased m rna and protein expression of foxc1, pi3k, akt, nf-κb, cyclin d1 and tgf-β1, a decreased expression of p-akt, suppressed cell proliferation, accelerated apoptosis, and an increased number of cells at the g0/g1 phase were observed following the upregulation of mi r-200a and downregulation of foxc1.Conclusion: the overexpression of mi r-200a may downregulate foxc1, thereby inhibiting the activation of the pi3k/akt signaling pathway and ultimately suppressing asmc proliferation and airway remodeling in asthmatic mice.This evidence supports the potential that mi r-200a represents a new approach to treating asthma.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Elevated Expression of Zinc Finger Protein 703 Promotes Cell Proliferation and Metastasis through PI3K/AKT/GSK-3β Signalling in Oral Squamous Cell Carcinoma

Zinc finger protein 703 (znf703), initially identified as a novel oncogene in human breast cancer, is a member of the net/nl z family of zinc finger transcription factors.It is recognized that the overexpression of znf703 is associated with various types of human cancers, but the role and molecular mechanism of znf703 in oral squamous cell carcinoma (oscc) are unknown.Methods: znf703 expression levels were examined in oscc tissues and non-cancerous tissues by q rt-pcr and immunohistochemistry (ihc).The molecular mechanisms of znf703 and its effects on cell growth and metastasis were explored in vitro and in vivo using the cck8 assay, colony formation assay, cell cycle analysis, migration and invasion assays, wound-healing assay, western blotting and xenograft experiments in nude mice.Results: in this study, znf703 was found to be upregulated in oscc tissues compared to that in normal tissues at both m rna and protein levels, and its expression level was closely correlated with the overall survival of patients with oscc.Silencing of the znf703 gene in oscc cells significantly inhibited cell growth and metastasis in vitro and in vivo.Conversely, the overexpression of znf703 in oscc cells promoted cancer growth and metastasis in vitro.Mechanistically, znf703 activated the pi3k/akt/gsk-3β signalling pathway and its downstream effectors, thus regulating the cell cycle and epithelial-mesenchymal transition (emt).Furthermore, the promotive effects of znf703 on cellular proliferation and metastasis could be rescued by ly294002 (a pi3k-specific inhibitor) and mk2206 (an akt-specific inhibitor).Conclusion: the results show that znf703 promotes cell growth and metastasis through pi3k/akt/gsk-3β signalling in oscc and that it may be a promising target in the treatment of patients with oscc.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

Myocardial infarction (mi) is a leading cause of morbidity and mortality.Here, we sought to explore the potential role and underlying mechanism of mi r-145 in mi.Methods: h9c2 cells were cultured under persistent hypoxia to simulate mi.The hypoxia-induced injury was assessed on the basis of cell viability, migration, invasion and apoptosis.The expression of mi r-145 was evaluated by q rt-pcr and the influence of aberrantly expressed mi r-145 on h9c2 cells under hypoxia was also estimated.Utilizing bioinformatics methods, the target genes of mi r-145 were verified by luciferase reporter assay.Then, effects of abnormally expressed target gene on mi r-145 silenced h9c2 cells were assessed.Finally, the phosphorylation levels of key kinases in the phosphatidylinositol-3-kinase (pi3k)/akt and the mitogen-activated protein kinase (mapk)/extracellular signal-regulated kinase (erk) pathways were detected by western blot analysis.Results: hypoxia remarkably lowered viability, migration and invasion but promoted cell apoptosis.Meantime, the mi r-145 level was up-regulated in h9c2 cells under hypoxia.Following experiments suggested that hypoxia-induced injury was exacerbated by mi r-145 overexpression while was alleviated by mi r-145 silence.Rac1 was predicted and further validated to be a target gene of mi r-145.The influence of mi r-145 silencing on h9c2 cells under hypoxia could be reversed by down-regulation of rac1.Additionally, the phosphorylation levels of pi3k, akt, mapk and erk were all elevated in mi r-145 silenced cells and these alterations were reversed by down-regulation of rac1.Conclusion: mi r-145 silencing could protect h9c2 cells against hypoxia-induced injury by targeting rac1, in which pi3k/akt and mapk/erk pathways might be involved.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
CXCL16 protects against oxygen and glucose deprivation‐induced injury in human microvascular endothelial cells‐1: Potential role in ischemic stroke

Aim to explore the protective effect of chemokine ligand 16 (cxcl16) against cell damage induced by oxygen‐glucose deprivation (ogd) in human microvascular endothelial cells‐1 (hmec‐1) and its possible mechanism.Methods cell counting kit‐8 (cck‐8) assay and flow cytometry were performed to determine cell viability and apoptosis of hmec‐1, respectively.Q rt‐pcr analysis was applied to display the expression of cxcl16 and mi r‐424.Western blot analysis was used to detect the expression of apoptosis‐related proteins, cxcl16, c amp/pka/creb, and pi3k–akt–gsk3β pathway‐related proteins.Results ogd significantly inhibited cell viability and promoted apoptosis.Cxcl16 overexpression decreased the proliferation inhibition and apoptosis of hmec‐1 induced by ogd.Furthermore, we found that cxcl16 was a target of mi r‐424 and was downregulated by mi r‐424.The further study showed that overexpression of mi r‐424 significantly increased proliferation inhibition and apoptosis of hmec‐1 induced by ogd.In addition, we also found that mi r‐424 was downregulated by pms2l2.In the subsequence experiment, overexpression of pms2l2 significantly decreased the proliferation inhibition and apoptosis of hmec‐1 induced by ogd, which suggested that pms2l2 decreased cell damage of hmec‐1 induced by ogd.Simultaneously, cxcl16 treatment markedly increased the phosphorylation of pka/creb and pi3k–akt–gsk3β and these signal pathways were blocked by signal inhibitors.Conclusion our study first demonstrates that oxygen‐glucose deprivation (ogd)‐induced human microvascular endothelial cells‐1 (hmec‐1) cell injury was alleviated by cxcl16 targeted by mi r‐424 which further targeted by pms2l2.This process might also be regulated by activating pka/creb and pi3k–akt–gsk3β pathways.

Journal: Journal of Cellular Physiology (2019)
Publication types: Research Article;
The circular RNA HIPK3 reduces hydrogen peroxide‐induced injury of PC‐12 cells by upregulation of miR‐455

The above article, ‘the circular rna hipk3 reduces hydrogen peroxide‐induced injury of pc‐12 cells by upregulation of mi r‐455’, by xuming chen, jie chen, senjun jin, guangzhao yan, chaozhou hu, shengan hu published online on 21 january 2020 in wiley online library ( ), has been retracted by agreement between the authors, the journal acting editor in chief, dr.Lucie kalvodova, and the wiley periodicals llc.Following an investigation based on public allegations.The authors stated that the experimental data in the article could not be reproduced.

Journal: Journal of Cellular Biochemistry (2020)
Publication types: Research Article;
Beta‐elemene increases chemosensitivity to 5‐fluorouracil through downregulating microRNA‐191 expression in colorectal carcinoma cells

Colorectal carcinoma is a common malignant tumor occurring in the alimentary system.Despite developments of modern medicine, developed resistance to 5‐fluorouracil (5‐fu) may lead to poor prognosis.Herein, we aimed to explore the effects of beta‐elemene on colorectal carcinoma cells (hct116 and ht29) as well as the underlying mechanisms.Beta‐elemene reduced cell viability and induced apoptosis in hct116 and ht29 cells.Increased apoptosis following beta‐elemene exposure was due to enhanced sensitivity to 5‐fu through down‐regulating mi r‐191.Expression of key kinases, including wnt3a, and β‐catenin, were down‐regulated by beta‐elemene through a mi r‐191 mechanism.Moreover, beta‐elemene might improve resistance of colorectal carcinoma cells to 5‐fu by down‐regulating mi r‐191, thereby inhibiting the wnt/β‐catenin pathway.

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