MicroRNA‑302a inhibits cell proliferation and invasion, and induces cell apoptosis in hepatocellular carcinoma by directly targeting VEGFA
| Autor: | Chen Wang, Wen-Zhang Zha, Yong-Hua Xu, Hui-Min Ding, Cheng-Lin Qin, Ren-Gen Fan |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Oncology Male Vascular Endothelial Growth Factor A Cancer Research Cell Biochemistry 0302 clinical medicine Cell Movement RNA Small Interfering Liver Neoplasms Hep G2 Cells Cell cycle Middle Aged Gene Expression Regulation Neoplastic Vascular endothelial growth factor A medicine.anatomical_structure 030220 oncology & carcinogenesis Lymphatic Metastasis Molecular Medicine Female A431 cells Signal Transduction Adult medicine.medical_specialty Carcinoma Hepatocellular Biology 03 medical and health sciences Internal medicine Cell Line Tumor microRNA Genetics medicine Humans neoplasms Molecular Biology Aged Cell Proliferation Neoplasm Staging Oligoribonucleotides Oncogene Cell growth Cancer Antagomirs medicine.disease digestive system diseases MicroRNAs 030104 developmental biology Neoplasm Grading |
| Zdroj: | Molecular medicine reports. 16(5) |
| ISSN: | 1791-3004 |
| Popis: | Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third most common cause of cancer‑related mortality worldwide. An increasing number of studies have demonstrated that microRNAs may be used as diagnostic, therapeutic and prognostic targets for human cancers, including HCC. The present study aimed to evaluate microRNA (miR)‑302a expression and function in HCC, and its underlying mechanisms. The results revealed that miR‑302a was expressed at low levels in HCC tissues and cell lines. Reduced miR‑302a expression was correlated with tumor‑node‑metastasis stage and lymph node metastasis in patients with HCC. Additionally, overexpression of miR‑302a reduced cell proliferation and invasion, and induced apoptosis in HCC cells. Vascular endothelial growth factor A (VEGFA) was demonstrated to be a direct target gene of miR‑302a. VEGFA was highly expressed in HCC tissues and inversely correlated with miR‑302a expression. Knockdown of VEGFA expression led to reduced HCC cell proliferation and invasion, and increased apoptosis rates, similar to miR‑302a overexpression, which suggested that VEGFA may be a functional downstream target of miR‑302a in HCC. These data suggested that this newly identified miR‑302a/VEGFA axis may be involved in HCC formation and progression. The present results also provide novel potential targets for the treatments of patients with HCC. |
| Databáze: | OpenAIRE |
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