Baotong Xie1, Zhaohua Wang1, Tao Li2, Junfang Xue1, Chunming Zhang3. 1. Department of Otolaryngology, Lvliang People's Hospital, The Affiliated Lvliang Hospital of Shanxi Medical University Lvliang, Shanxi, China. 2. Department of Ophthalmology, Lvliang People's Hospital, The Affiliated Lvliang Hospital of Shanxi Medical University Lvliang, Shanxi, China. 3. Department of Otolaryngology and Head-neck Surgery, First Hospital of Shanxi Medical University Taiyuan, Shanxi, China.
Abstract
OBJECTIVE: To investigate the mechanism of lncRNA MALAT1 (MALAT1) inhibiting the proliferation and invasiveness of laryngeal squamous cell carcinoma (LSCC) Hep-2 cells by modulating miR-362-3p. METHODS: We collected the expression profile of lncRNAs and miRNAs in LSCC downloaded from The Cancer Genome Atlas (TCGA) database as well as LSCC tissue samples and adjacent normal counterparts resected from LSCC patients in Lvliang People's Hospital and First Hospital of Shanxi Medical University between January 2018 and June 2020 for analysis. Human LSCC Hep-2 cells were selected for experiments. The expression of miR-362-3p and MALAT1 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cells were subsequently transfected to knock out MALAT1, and the growth, metastasis and invasiveness of cells were evaluated by CCK-8 assay, plate clone formation, wound healing, and Transwell invasion assays respectively. The binding of MALAT1 to miR-362-3p was verified by RNA pull-down, RNA binding protein immunoprecipitation (RIP), and dual-luciferase reporter assays. RESULTS: MALAT1 was highly expressed while miR-362-3p was lowly expressed in both LSCC tissues and cells compared with normal counterparts. MALAT1 knockdown inhibited the viability of Hep-2 cells, reducing the number of plate clone-forming cells as well as the number of migrated and invaded cells. Transfection of miR-362-3p inhibitor into Hep-2 cells treated by si-MALAT1 reversed the inhibition of si-MALAT1 on the proliferation of Hep-2 cells, and promoted cell invasiveness and migration. MALAT1 can sponge miR-362-3p and inhibit its expression. CONCLUSIONS: Knockdown of MALAT can inhibit Hep-2 cell proliferation and reduce its invasiveness and migration by modulating miR-362-3p. AJTR
OBJECTIVE: To investigate the mechanism of lncRNA MALAT1 (MALAT1) inhibiting the proliferation and invasiveness of laryngeal squamous cell carcinoma (LSCC) Hep-2 cells by modulating miR-362-3p. METHODS: We collected the expression profile of lncRNAs and miRNAs in LSCC downloaded from The Cancer Genome Atlas (TCGA) database as well as LSCC tissue samples and adjacent normal counterparts resected from LSCC patients in Lvliang People's Hospital and First Hospital of Shanxi Medical University between January 2018 and June 2020 for analysis. Human LSCC Hep-2 cells were selected for experiments. The expression of miR-362-3p and MALAT1 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cells were subsequently transfected to knock out MALAT1, and the growth, metastasis and invasiveness of cells were evaluated by CCK-8 assay, plate clone formation, wound healing, and Transwell invasion assays respectively. The binding of MALAT1 to miR-362-3p was verified by RNA pull-down, RNA binding protein immunoprecipitation (RIP), and dual-luciferase reporter assays. RESULTS: MALAT1 was highly expressed while miR-362-3p was lowly expressed in both LSCC tissues and cells compared with normal counterparts. MALAT1 knockdown inhibited the viability of Hep-2 cells, reducing the number of plate clone-forming cells as well as the number of migrated and invaded cells. Transfection of miR-362-3p inhibitor into Hep-2 cells treated by si-MALAT1 reversed the inhibition of si-MALAT1 on the proliferation of Hep-2 cells, and promoted cell invasiveness and migration. MALAT1 can sponge miR-362-3p and inhibit its expression. CONCLUSIONS: Knockdown of MALAT can inhibit Hep-2 cell proliferation and reduce its invasiveness and migration by modulating miR-362-3p. AJTR
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