miR-29a-3p inhibits endometrial cancer cell proliferation, migration and invasion by targeting VEGFA/CD C42/PAK1

Geng, Aizhi; Lin, Li‐Rong; Ren, Fengyun; Zhang, Ling; Zhou, Haiying; Xue, Guanhua

doi:10.1186/s12885-021-08506-z

Cited by 21 publications

(16 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The VEGF family consists of cytokines known to be angiogenic factors that participate in blood vessel formation and lymphangiogenesis (30). VEGFA is the main member of this family of proteins, which has been revealed to regulate cell proliferation, apoptosis and invasion (11)(12)(13)31,32). In particular, VEGFC has also been reported to impact the progression of hemangioma (22).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA‑203a‑3p suppresses endothelial cell proliferation and invasion, and promotes apoptosis in hemangioma by inactivating the VEGF‑mediated PI3K/AKT pathway

Zhuo

et al. 2022

Exp Ther Med

View full text Add to dashboard Cite

Our previous study demonstrated that was involved in the regulation of long non-coding RNA MEG8-mediated the progression of hemangioma, which is a benign tumor characterized by endothelial hyperplasia in the blood vessels and primarily occurring in infants and females. Therefore, the present study aimed to further investigate the effects of miR-203a-3p on endothelial cell proliferation, invasion and apoptosis, as well as its underlying mechanism in hemangioma. Human hemangioma endothelial cells (HemECs) were first transfected with either miR-203a-3p mimics or a miR-203a-3p inhibitor. Subsequently, vascular endothelial growth factor A (VEGFA) was overexpressed in these cells. Cell proliferation (by Cell Counting Kit-8 assay), apoptosis (by TUNEL assay), invasion (by Transwell assay) and PI3K/AKT signaling (by western blot) were assessed following transfection of these cells. Notably, transfection with miR-203a-3p mimics caused a reduction in cell proliferation, invasion and in the phosphorylation levels of PI3K and AKT, and promoted cell apoptosis in HemECs. By contrast, transfection with the miR-203a-3p inhibitor exerted the opposite effects compared with those of the miR-203a-3p mimics. miR-203a-3p was revealed to directly suppress VEGFA expression in HemECs. VEGFA overexpression alone increased cell proliferation and invasion, but decreased apoptosis. Furthermore, VEGFA co-transfection reversed the effects mediated by miR-203a-3p mimics transfection in HemECs. Mechanistically, miR-203a-3p was demonstrated to inactivate the PI3K/AKT pathway, whereas VEGFA overexpression produced the opposite effect. VEGFA co-transfection also attenuated the miR-203a-3p mimics-induced inactivation of PI3K/AKT signaling in HemECs. In conclusion, these data suggested that miR-203a-3p may inhibit endothelial cell proliferation and invasion, and promote apoptosis by inactivating VEGFA and PI3K/AKT signaling in hemangioma. These findings also implicated miR-203 as a possible treatment option for this disease.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Vascular epithelial growth factor A (VEGFA) is a critical regulator of a number of cellular processes, including proliferation, apoptosis and invasion (11)(12)(13). Notably, it has been demonstrated that VEGFA can serve a role in the pathogenesis of hemangioma in several ways, including through the promotion of angiogenesis (14).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑203a‑3p suppresses endothelial cell proliferation and invasion, and promotes apoptosis in hemangioma by inactivating the VEGF‑mediated PI3K/AKT pathway

Zhuo

et al. 2022

Exp Ther Med

View full text Add to dashboard Cite

show abstract

“…30 Geng et al reported that miR-29a-3p inhibited the proliferation, migration, and invasion of endometrial cancer cells by targeting VEGFA/CDC42/PAK1. 31 In addition, it has also been concluded that miR-29a-3p could inhibit the migration ability and proliferation of cervical cancer cells by directly targeting SNIP1. 32 Based on lncRNA HOXA-AS3 interacting with miR-29a-3p, the molecular mechanism of cervical cancer was deeply explored in this study.…”

Section: Discussionmentioning

confidence: 99%

Prognostic value of lncRNA HOXA‐AS3 in cervical cancer by targeting miR‐29a‐3p and its regulatory effect on tumor progression

Tang

et al. 2022

J of Obstet and Gynaecol

View full text Add to dashboard Cite

Background: With the promotion of human papillomavirus (HPV) vaccine, cervical cancer has become a current research hotspot, and lncRNA has been confirmed to be used in the research of different diseases. This article systematically expounds the regulation and potential mechanisms of HOXA cluster antisense RNA 3 (HOXA-AS3) in cervical cancer, and discusses its possibility as a prognostic biomarker for cervical cancer. Methods: Relative expression levels of HOXA-AS3 and miR-29a-3p in tissues and cells were determined by real-time quantitative polymerase chain reaction (RT-qPCR). The survival of cervical cancer patients was analyzed by Kaplan-Meier method and the cumulative survival function table was drawn. The proliferation, migration, and invasion levels of HOXA-AS3 in cells were detected according to cell counting kit-8 (CCK-8) and transwell method. The dual-luciferase reporter gene assay confirmed the mechanism of action between HOXA-AS3 and miR-29a-3p. Results: HOXA-AS3 was elevated and miR-29a-3p was decreased in tissues and cells of cervical cancer patients. Knockdown of HOXA-AS3 could inhibit the progression of cervical cancer and was more conducive to patient survival. Bioinformatics analysis confirmed that HOXA-AS3 negatively regulates cervical cancer development by sponging miR-29a-3p. Conclusion:In this research, knockdown of HOXA-AS3 could alleviate the process of cervical cancer by sponging miR-29a-3p, suggesting that HOXA-AS3 may be a potential prognostic target of cervical cancer, which could provide a theoretical basis for future clinical research of cervical cancer.

show abstract

“…Many studies have reported that aberrant expression of miR-29a-3p is involved in the development of many diseases. For example, in endometrial cancer, miR-29a-3p inhibits cell proliferation, migration and invasion by targeting VEGFA/CDC42/PAK1 signaling pathway ( 13 ). MiR-29a-3p suppressed the migration and proliferation of HeLa cells by directly targeting SNIP1 ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

“…MiR-29a-3p, reporte-dly, is a pivotal regulator in cancer biology. Specifically, miR-29a-3p dysregulation takes part in the progression of certain cancers, such as osteosarcoma ( 11 ), breast cancer ( 12 ), endometrial cancer ( 13 ), hepatocellular carcinoma ( 14 ). Instead, the role of miR-29a-3p in ONFH and SAON is unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR-29a-3p Inhibits Proliferation and Osteogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells via Targeting FOXO3 and Repressing Wnt/β-Catenin Signaling in Steroid-Associated Osteonecrosis

et al. 2022

View full text Add to dashboard Cite

Background and Objectives: This study was to investigate the role of microRNA-29a-3p (miR-29a-3p) in human bone marrow mesenchymal stem cells (hBMSCs), and its relationship with steroid-associated osteonecrosis. Methods and Results: The online tool GEO2R was used to screen out the differentially expressed genes (DEGs) in GSE123568 dataset. Quantitative real time-polymerase chain reaction (qRT-PCR) was performed to detect the expression of miR-29a-3p, forkhead box O3 (FOXO3), alkaline phosphatase (ALP), bone gamma-carboxyglutamate protein (OCN) and RUNX family transcription factor 2 (Runx2) in the hBMSCs isolated from the patients with steroid-associated osteonecrosis. CCK-8 assay was executed to measure cell viability; western blot assay was utilized to detect FOXO3, ALP, Runx2, OCN and β-catenin expression. Cell apoptosis and cell cycle were detected by flow cytometry. Immunofluorescence assay was used to detect the sub-cellular localization of β-catenin. Bioinformatics analysis and luciferase reporter gene assay were performed to confirm whether miR-29a-3p can combine with FOXO3 3'UTR. MiR-29a-3p was markedly up-regulated in the hBMSCs of patients with steroid-associated osteonecrosis, while FOXO3 mRNA was significantly down-regulated. Transfection of miR-29a-3p mimics significantly inhibited the hBMSCs' proliferation, osteogenic differentiation markers' expressions, including ALP, Runx2, OCN, and repressed the ALP activity, as well as promoted cell apoptosis and cell-cycle arrest. FOXO3 was identified as a target gene of miR-29a-3p, and miR-29a-3p can inhibit the expression of FOXO3 and β-catenin, and inhibition of miR-29a-3p promoted translocation of β-catenin to the nucleus. Conclusions: MiR-29a-3p can modulate FOXO3 expression and Wnt/β-catenin signaling to inhibit viability and osteogenic differentiation of hBMSCs, thereby promoting the development of steroid-associated osteonecrosis.

show abstract

miR-29a-3p inhibits endometrial cancer cell proliferation, migration and invasion by targeting VEGFA/CD C42/PAK1

Cited by 21 publications

References 36 publications

MicroRNA‑203a‑3p suppresses endothelial cell proliferation and invasion, and promotes apoptosis in hemangioma by inactivating the VEGF‑mediated PI3K/AKT pathway

MicroRNA‑203a‑3p suppresses endothelial cell proliferation and invasion, and promotes apoptosis in hemangioma by inactivating the VEGF‑mediated PI3K/AKT pathway

Prognostic value of lncRNA HOXA‐AS3 in cervical cancer by targeting miR‐29a‐3p and its regulatory effect on tumor progression

MiR-29a-3p Inhibits Proliferation and Osteogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells via Targeting FOXO3 and Repressing Wnt/β-Catenin Signaling in Steroid-Associated Osteonecrosis

Contact Info

Product

Resources

About