MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

Tao, Tieying; Shen, Qinrong; Luo, Jianmin; Xu, Youzhi; Liang, Wenqing

doi:10.1159/000481560

Cited by 23 publications

(21 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated that miRNAs are aberrantly expressed in various cancers such as lung cancer, liver cancer, and gastric cancer . MicroRNA‐125a (MiR‐125a), located on chromosome 19q13, is a member of the miR‐125 family and has been reported as a potential tumor suppressor in multiple cancers by targeting different genes, such as osteosarcoma, ovarian cancer, breast cancer, lung cancer, and glioma . However, little is known about the expression profile and functional roles of miR‐125a in RCC.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐125a suppresses cell migration, invasion, and regulates hyaluronic acid synthase 1 expression by targeting signal transducers and activators of transcription 3 in renal cell carcinoma cells

Sun

Guo

Yao

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Renal cell carcinoma (RCC) is one of the most common cancers in urology. MicroRNA-125a (miR-125a) has been demonstrated to be implicated in various cancers. However, the functional role of miR-125a in RCC remains largely unclear. This study was aimed to investigate the functional role of miR-125a and the expression relevance of signal transducers and activators of transcription 3 (STAT3) with hyaluronic acid synthase 1 (HAS1) in RCC. We revealed that miR-125a was downexpressed in 786-O cells, and examined transfected efficiency. According to functional assay, overexpression of miR-125a inhibited cell migration and cell invasion, but no obvious effect was observed on cell proliferation. The luciferase activity assay showed that miR-125a could directly target STAT3 3'-untranslated regions. Meanwhile, quantitative polymerase chain reaction (qPCR) assay and Western blot analysis demonstrated that miR-125a could inhibit STAT3 expression at both messenger RNA and protein levels. Furthermore, the combination sites between STAT3 and HAS1 were predicted by prediction of transcription factor binding sites database analysis. The expression of STAT3 was correlated with HAS1 expression, exemplified by the same tendency detected by qPCR assay. Taken together, our results preliminarily demonstrate that miR-125a could constrain cell migration, invasion, and regulate HAS1 expression in RCC cells by targeting STAT3. It is likely to facilitate a better understanding of the regulation mechanisms of miR-125a in RCC.

show abstract

Section: Introductionmentioning

confidence: 99%

MicroRNA‐125a suppresses cell migration, invasion, and regulates hyaluronic acid synthase 1 expression by targeting signal transducers and activators of transcription 3 in renal cell carcinoma cells

Sun

Guo

Yao

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…reported that overexpressed E2F2 is closely related to poor post progression survival in ovarian cancer patients, and can be used for targeted treatment and prognosis prediction [5]. Similar results can be found in glioma [6] osteosarcoma [7], gastric cancer [8] and melanoma [9], it's not surprising that E2F2 is regarded as oncogene. However, E2F2 is a suppressor gene in clear cell renal cell carcinoma [10] and Tcell lymphoma [11].…”

Section: Introductionmentioning

confidence: 67%

Increased E2F2 predicts poor prognosis in patients with HCC based on TCGA data

Zeng

Cao

Tang³

2020

Preprint

View full text Add to dashboard Cite

Background: The E2F family of transcription factor 2 (E2F2) plays an important role in the development and progression of various tumors, but its association with hepatocellular carcinoma remains unknown. The aim of our study was to investigate the role and clinical significance of E2F2 in hepatocellular carcinoma (HCC).Methods: HCC raw data were extracted from The Cancer Genome Atlas (TCGA). Wilcoxon signed-rank test, Kruskal-Wallis test and logistic regression was applied to analyze the relationship between the expression of E2F2 and clinicopathologic characteristics. Cox regression and Kaplan-Meier was employed to evaluate the correlation between clinicopathologic features and survival. The biological function of E2F2 was annotated by Gene set enrichment analysis (GSEA).Results: The expression of E2F2 was increased in HCC samples. The expression of elevated E2F2 in HCC samples was prominently correlated with histologic grade (OR =2.62 for G3-4 vs. G1-2, p=1.80E-05), clinical stage (OR =1.74 for III-IV vs. I-II, p=0.03), T (OR =1.64 for T3-4 vs.T1-2, p=0.04), tumor status (OR =1.88 for with tumor vs. tumor free, p= 3.79E-03), plasma alpha fetoprotein (AFP) value (OR =3.18 for AFP≥400 vs AFP＜20, p= 2.16E-04; OR=2.50 for 20≤AFP＜400 vs AFP＜20, p=2.56E-03). Increased E2F2 had an unfavorable OS (p=7.468e−05), PFI (p=3.183e−05), DFI (p=0.001), DSS (p=4.172e−05). Elevated E2F2 was independently bound up with OS (p =0.004 , hazard ratio [HR]= 2.4 (95% CI [1.3-4.2])), DFI (P =0.029, hazard ratio [HR] = 2.0 (95% CI [1.1-3.7])) and PFI (P =0.005, hazard ratio [HR] = 2.2 (95% CI [1.3-3.9])) . GSEA disclosed that cell circle, RNA degradation, pyrimidine metabolism, base excision repair, aminoacyl tRNA biosynthesis, DNA replication, p53 signaling pathway, nucleotide excision repair, ubiquitin mediated proteolysis, citrate cycle TCA cycle were notably enriched in E2F2 high expression phenotype.Conclusions: Elevated E2F2 can be a promising independent prognostic biomarker and therapeutic target for HCC. Additionally, cell cycle, pyrimidine metabolism, DNA replication, p53 signaling pathway, ubiquitin mediated proteolysis, the citrate cycle TCA cycle may be the key pathway by which E2F2 participate in the initial and progression of HCC.

show abstract

“…Quan Zhou et al reported that overexpressed E2F2 is closely related to poor post progression survival in ovarian cancer patients, and can be used for targeted treatment and prognosis prediction (4). Similar results can be found in glioma (5),osteosarcoma (6), gastric cancer (7) and melanoma (8), it's not surprising that E2F2 is regarded as oncogene. However, E2F2 is a suppressor gene in clear cell renal cell carcinoma (9) and T-cell lymphoma (10).…”

Section: Introductionmentioning

confidence: 75%

Increased E2F2 predicts poor prognosis in patients with HCC based on TCGA data

Zeng

Cao

Tang³

2020

Preprint

View full text Add to dashboard Cite

Background E2F transcription factor 2(E2F2) plays an important role in the development and progression of various tumors, but its association with hepatocellular carcinoma remains unknown.The aim of our study was to investigate the role and clinical significance of E2F2 in hepatocellular carcinoma (HCC). Methods HCC raw data were extracted from TCGA. Wilcoxon signed-rank test, Kruskal-Wallis test and logistic regression was applied to analyze the the relationship between the expression of E2F2 and clinicalpathologic charateristics. Cox regression and Kaplan-Meier was employed to evaluate the correlation between clinicopathologic features and survial. The biological function of E2F2 was annotated by Gene set enrichment analysis (GSEA). Results The expression of E2F2 was increased in HCC samples. The expression of elevated E2F2 in HCC samples was prominentlly correlated with tumor grade (OR =2.62 for G3-4 vs. G1-2, p=1.80E-05), tumor stage (OR =1.74 for III-IV vs. I-II, p=0.03), topography (OR =1.64 for T3-4 vs.T1-2, p=0.04), tumor status (OR =1.88 for with tumor vs. tumor free, p= 3.79E-03), plasma AFP value (OR =3.18 for AFP≥400 vs AFP<20, p= 2.16E-04; OR=2.50 for 20≤AFP<400 vs AFP<20, p=2.56E-03). Increased E2F2 had a unfavorable OS (p=7.468e−05), PFI (p=3.183e−05), DFI (p=0.001), DSS (p=4.172e−05). Elevated E2F2 was independently bound up with OS (p = 4.4E-04, HR = 2.4 (95% CI [1.5-3.8])) and DSS (p = 7.6E-04, HR = 3.0, (95% CI [1.6-5.6])). GSEA disclosed that cell circle, RNA degradation, pyrimidine metabolism, base excision repair, aminoacyl tRNA biosynthesis, DNA replication, p53 signalling pathway, nucleotide excision repair, ubiquitin mediated proteolysis, citrate cycle TCA cycle were notably enriched in E2F2 high expression phenotype. Conclusions Elevated E2F2 can be a promissing independent prognostic biomarker and therapeutic target for HCC. Additionally, cell cycle, pyrimidine metabolism, DNA replication, p53 signalling pathway, ubiquitin mediated proteolysis, the citrate cycle TCA cycle may be the key pathway by which E2F2 participate in the initial and progression of HCC.

show abstract

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

Cited by 23 publications

References 31 publications

MicroRNA‐125a suppresses cell migration, invasion, and regulates hyaluronic acid synthase 1 expression by targeting signal transducers and activators of transcription 3 in renal cell carcinoma cells

MicroRNA‐125a suppresses cell migration, invasion, and regulates hyaluronic acid synthase 1 expression by targeting signal transducers and activators of transcription 3 in renal cell carcinoma cells

Increased E2F2 predicts poor prognosis in patients with HCC based on TCGA data

Increased E2F2 predicts poor prognosis in patients with HCC based on TCGA data

Contact Info

Product

Resources

About