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LINC00662 promotes glycolysis and cell survival by regulating miR- 375/HIF-1α axis in ovarian cancer.

厌氧糖酵解 瓦博格效应 乳酸脱氢酶A 小RNA 癌细胞 癌症 化学 巴基斯坦卢比 细胞 细胞生物学 转移 基因敲除 PI3K/AKT/mTOR通路 细胞凋亡 细胞培养
作者
L M Tao,Yan Gong,H. J. Yang,J H Pei,Xiu Song Zhao,Shuai Liu
出处
期刊:PubMed 卷期号:34 (3): 467-477 被引量:6
标识
DOI:10.23812/19-300-a-18
摘要

Ovarian cancer (OC) is one of the most common gynecological malignancies, with the highest mortality rate in women worldwide. LINC00662, a long non-coding RNA (lncRNA), was shown to play a vital role in many malignancies, while little is known about its role in OC. Firstly, our study determined the expression of LINC00662 in OC tissues and cells. Upregulation or downregulation of LINC00662 were performed in OC cells to explore its effects on cell proliferation and glycolysis of OC. The interaction between LINC00662 and miR-375 was verified using luciferase assays and RNA immunoprecipitation. Results showed that LINC00662 was highly expressed in OC tissues and cells, and patients with increased expression of LINC00662 were associated with shorter overall survival. Furthermore, functional assays proved that LINC00662 was essential for OC cell proliferation and glycolysis. Subsequently, our study further revealed that LINC00662 acted as a competitive RNA and it could modulate the expression of HIF-1α through directly binding with miR- 375. Collectively, upregulation of LINC00662 in ovarian cancer tissues is closely correlated to poor survival. LINC00662 might regulate HIF-1α expression via miR-375. These findings suggested that LINC00662 has the potential to be explored as a diagnostic biomarker for OC.

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