Yu Wang1, Qigang Zhang2. 1. Department of Thoracic Surgery, the Second Hospital of Dalian Medical University, Dalian, China. 2. Department of Thoracic Surgery, the First Hospital of China Medical University, Shenyang, China.
Abstract
Background: Long noncoding RNAs (lncRNAs) and mRNAs (messenger RNAs) have been reported to exert function in non-small-cell lung cancer (NSCLC), but how lncRNAs and mRNAs operate in the regulation of NSCLC is unclear. The purpose of this research was to elucidate the functional mechanism of lncRNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and tripartite-motif protein family member 65 (TRIM65) in NSCLC. Materials and Methods: Quantitative real-time polymerase chain reaction and western blot assay were employed to measure gene expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were performed to assess cell proliferation and apoptosis, respectively. Also, cell migratory and invasive abilities were detected by transwell assay. The interaction between miR-515-5p and MALAT1 or TRIM65 was predicted by starBase and then confirmed with the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay, or pull-down assay. Besides, mouse xenograft was conducted to analyze the effect of MALAT1 knockdown on tumor growth in vivo. Results: MALAT1 and TRIM65 expression was upregulated, and miR-515-5p expression was downregulated in NSCLC tissues and cells. Both MALAT1 knockdown and TRIM65 depletion suppressed cell proliferation, migration, and invasion and induced apoptosis in NSCLC cells. Interestingly, MALAT1 directly inhibited miR-515-5p expression and miR-515-5p decreased TRIM65 level through interaction. MALAT1 knockdown repressed NSCLC cell growth via modulation of miR-515-5p/TRIM65 axis. Furthermore, silencing MALAT1 inhibited tumor growth in vivo. Conclusions: Our findings demonstrated that MALAT1 depletion inhibited the growth of NSCLC cells by regulating miR-515-5p/TRIM65 axis, providing the theoretical basis for the therapy of NSCLC.
Background: Long noncoding RNAs (lncRNAs) and mRNAs (messenger RNAs) have been reported to exert function in non-small-cell lung cancer (NSCLC), but how lncRNAs and mRNAs operate in the regulation of NSCLC is unclear. The purpose of this research was to elucidate the functional mechanism of lncRNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and tripartite-motif protein family member 65 (TRIM65) in NSCLC. Materials and Methods: Quantitative real-time polymerase chain reaction and western blot assay were employed to measure gene expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were performed to assess cell proliferation and apoptosis, respectively. Also, cell migratory and invasive abilities were detected by transwell assay. The interaction between miR-515-5p and MALAT1 or TRIM65 was predicted by starBase and then confirmed with the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay, or pull-down assay. Besides, mouse xenograft was conducted to analyze the effect of MALAT1 knockdown on tumor growth in vivo. Results:MALAT1 and TRIM65 expression was upregulated, and miR-515-5p expression was downregulated in NSCLC tissues and cells. Both MALAT1 knockdown and TRIM65 depletion suppressed cell proliferation, migration, and invasion and induced apoptosis in NSCLC cells. Interestingly, MALAT1 directly inhibited miR-515-5p expression and miR-515-5p decreased TRIM65 level through interaction. MALAT1 knockdown repressed NSCLC cell growth via modulation of miR-515-5p/TRIM65 axis. Furthermore, silencing MALAT1 inhibited tumor growth in vivo. Conclusions: Our findings demonstrated that MALAT1 depletion inhibited the growth of NSCLC cells by regulating miR-515-5p/TRIM65 axis, providing the theoretical basis for the therapy of NSCLC.
Entities:
Keywords:
MALAT1; TRIM65; cell growth; miR-515-5p; non-small-cell lung cancer