Inhibition of malignant biological behaviors of non-small cell lung cancer H1299 cells by long non-coding RNA00511 and its possible mechanisms
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Abstract:
[Abstract] Objective: To investigate the effects of long non-coding RNA LINC00511 (LINC00511) knockdown on the proliferation, apoptosis, invasion, and other malignant biological behaviors of non-small cell lung cancer (NSCLC) cells through bioinformatics analysis, in vivo and in vitro experiments, and to preliminarily explore its underlying mechanisms. Methods: The gene Expression profiling Interaction analysis (GEPIA) database was used to analyze the expression level of LINC00511 in NSCLC, and its correlation with clinical characteristics such as tumor stage and survival period of patients, as well as genes related to the malignant biological behaviors of tumor cells. The H1299 lung cancer cell line with LINC00511 knockdown was constructed using shRNA lentiviral vectors. The effects on the proliferation, migration, cell cycle and apoptosis of H1299 cells were detected by clone formation assay, scratch healing assay and flow cytometry, respectively. The expressions of related regulatory genes were detected by qRT-PCR, and the expressions of tumor-related proteins were detected by WB assay. A subcutaneous transplanted tumor model was constructed in nude mice, and the tumor tissues were taken for immunohistochemical experiments to detect the expression of Ki67. Results: GEPIA database analysis showed that the expression level of LINC00511 was elevated in NSCLC tissues and correlated with the clinical stage of the disease (P < 0.05). LINC00511 was correlated with the expressions of CASP, CCNB1, CDK4 and other genes in lung cancer (P < 0.01). Knockdown of LINC00511 could inhibit cell colony formation and migration abilities, promote the apoptosis of lung cancer cells, and affect cell cycle progression (P < 0.05, P < 0.01). LINC00511 knockdown could down-regulate the expressions of CCNB, CDK4 and TGF-β1 genes in lung cancer cells (P < 0.01), but had no significant effect on the expressions of CCND1 and VEGFA genes. LINC00511 knockdown could inhibit the expressions of MMP9 and CTNNB1, and up-regulated the expression of CASP3 (P < 0.05, P < 0.01). In vivo experiments in nude mice confirmed that LINC00511 knockdown could inhibit Ki67 expression in transplanted tumor tissues (P < 0.01). Conclusion: LINC00511 is highly expressed in non-small cell lung cancer tissues and is correlated with the clinical stage of lung cancer and the expressions of multiple genes. LINC00511 Knockdown of LINC00511 can inhibit the malignant biological behaviors of lung cancer H1299 cells by affecting the expressions of related genes and proteins.