FOXO3-induced lncRNA LOC554202 contributes to hepatocellular carcinoma progression via the miR-485-5p/BSG axis

FOXO3公司 基因敲除 癌症研究 下调和上调 肝细胞癌 巴西金 竞争性内源性RNA 长非编码RNA 细胞凋亡 生物 转移 转录因子 医学 基因 内科学 癌症 遗传学 基质金属蛋白酶
作者
Lin Yang,Wan-Li Deng,Bao-Guo Zhao,Yao-Zhong Xu,Xiaowen Wang,Fang Yu,Haijuan Xiao
出处
期刊:Cancer Gene Therapy [Springer Nature]
卷期号:29 (3-4): 326-340 被引量:14
标识
DOI:10.1038/s41417-021-00312-w
摘要

Long non-coding RNAs (LncRNAs) have played very important roles in the malignancy behaviors of hepatocellular carcinoma (HCC). LncRNA LOC554202 (LOC554202) was a newly identified tumor-related lncRNA. However, its expression and function in HCC remained unknown. In this study, we firstly reported that LOC554202 expression was distinctly upregulated in HCC specimens and cell lines. Clinical assays indicated that increased LOC554202 expression had a diagnostic value for HCC patients and was positively associated with advanced stages and poor clinical prognosis. Additionally, forkhead box O3(FOXO3) could bind directly to the LOC554202 promoter region and activate its transcription. Functionally, we observed that knockdown of LOC554202 suppressed the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progress of HCC cells, and promoted apoptosis. Mechanistically, LOC554202 competitively bound to miR-485-5p and prevented the suppressive effects of miR-485-5p on its target gene basigin (BSG), which finally led to HCC metastasis, EMT, and docetaxel chemoresistance. Our data demonstrated that FOXO3-induced LOC554202 contributed to HCC progression by upregulating BSG via competitively binding to miR-485-5p, which suggested that the regulation of the FOXO3/LOC554202/miR-485-5p/BSG axis may have beneficial effects in the treatment of HCC.

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