Long non-coding RNA LINC01207 promotes cell proliferation and migration but suppresses apoptosis and autophagy in oral squamous cell carcinoma by the microRNA-1301-3p/lactate dehydrogenase isoform A axis

被引:25
作者
Lu, Xiaolin [1 ]
Chen, Liling [2 ,3 ]
Li, Yang [2 ]
Huang, Rong [2 ]
Meng, Xiangfeng [2 ]
Sun, Fangfang [2 ]
机构
[1] Nanjing Univ, Dept Maxillofacial Surg, Nanjing Stomatol Hosp, Med Sch, Nanjing, Peoples R China
[2] Nanjing Univ, Dept Prosthodont, Nanjing Stomatol Hosp, Med Sch, Nanjing, Peoples R China
[3] Pudong New Dist Hosp Tradit Chinese Med, Dept Prosthodont, Shanghai, Peoples R China
关键词
OSCC; autophagy; linc01207; miR-1301-3p; ldha; LACTATE-DEHYDROGENASE; CANCER PROGRESSION; GLYCOLYSIS;
D O I
10.1080/21655979.2021.1972784
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Long noncoding RNAs (lncRNAs) have been reported to participate in the progression of various cancers, including oral squamous cell carcinoma (OSCC). This study aims to find out whether lncRNA LINC01207 regulates the progression of OSCC. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was conducted to evaluate gene expression in OSCC cells and tissues. Cell viability, proliferation, migration, apoptosis, and autophagy were detected using Cell Counting Kit-8 (CCK-8), colony formation, Transwell assays, flow cytometry, and western blot analysis. Luciferase reporter and RNA immunoprecipitation (RIP) assays were conducted to assess the interactions among genes. We found that LINC01207 was overexpressed in OSCC cells and tissues. LINC01207 silencing inhibited OSCC cell proliferation and migration but promoted apoptosis and autophagy, and LINC01207 overexpression had an opposite result. LINC01207 interacted with microRNA-1301-3p (miR-1301-3p) while lactate dehydrogenase isoform A (LHDA) was targeted by miR1301-3p. Effects caused by LINC01207 downregulation on OSCC cells were reversed by overexpression of LDHA. Overall, LINC01207 promotes OSCC progression via the miR-1301-3p/LDHA axis
引用
收藏
页码:7780 / 7793
页数:14
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