Abstract：Objective: To investigate the pathogenesis of LINC01614 in promoting the proliferation and progression of lung squamous cell carcinoma cells. Methods: The relative expression levels of LINC01614 in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LSCC) biopsies (20 cases in each cancer group) and corresponding adjacent tissues (20 cases in each cancer group) were determined by RT-qPCR assay. As well in human immortalized lung epithelial cell line 16HBE cells, human lung squamous cell carcinoma cell line HCC95 cells and NCI-H226 cells, and human lung adenocarcinoma cell line A549 cells and H1299 cells, the relative expression levels of LINC01614 were also determined. Lentivirus-mediated knockdown/overexpression of LINC01614 and infected with HCC95 cells. Cells were divided into the control group, Lenti-shRNA MOCK group, Lenti-LINC01614 shRNA group, Lenti-vector group, and Lenti-LINC01614 OE group. The proliferation abilities of each group of cells were measured by CCK-8 assay. Phosphorylated (p-) PI3K and PI3K, p-Akt, and Akt levels were determined by Western blot. The colony formation abilities were determined by colony formation ability assay. In vivo tumor growth of each group of mice was measured by xenografts. The differences in survival rate of xenografts were measured by survival curve. Results: Compared with LSCC-adjacent tissues, the relative expression levels of LINC01614 in LSCC tissues were increased (P<0.05). Compared with LUAD tissues, the relative expression levels of LINC01614 in LSCC tissues were increased (P<0.05) (F=385.60, P<0.0001). Compared with 16HBE cell group, the relative expression levels of LINC01614 in HCC95 cell group, NCI-H226 cell group, A549 cell group and H1299 cell group were increased (P<0.05); Compared with HCC95 cell group, the relative expression levels of LINC01614 in NCI-H226 cell group, A549 cell group, and H1299 cell group were decreased (P<0.05) (F=347.60, P<0.0001). Compared with the control group, in the Lenti-LINC01614 shRNA group, the cell proliferation ability was decreased (P<0.05). The relative levels of p-PI3K and p-AKT were decreased (P<0.05). Cell colony formation ability decreased (P<0.05). In vivo tumor growth of xenografts was decreased (P<0.05). Compared with the control group, in the Lenti-LINC01614 OE group, the cell proliferation ability was enhanced (P<0.05). The relative levels of p-PI3K and p-AKT were increased (P<0.05); Cell colony formation ability was enhanced (P<0.05). In vivo tumor growth of xenografts was enhanced (P<0.05). The survival rate (%) of xenografts was decreased (Chi square=19.82, P=0.0005). Conclusion: The abnormally high expression of LINC01614 in LSCC tissues could activate the PI3K/Akt signaling pathway and promote the proliferation ability of LSCC cells and LSCC progression.
张石磊, 许晨, 王亚红, 刘文燕, 媛荣, 李蕊仙. LINC01614促进肺鳞状细胞癌细胞增殖及进展的致病机制研究[J]. 河北医学, 2025, 31(4): 543-549.
ZHANG Shilei, XU Chen, WANG Yahong, et al. The Study on the Pathological Mechanisms of LINC01614 in Promoting the Proliferation and Progression of Lung Squamous Cell Carcinoma Cells. HeBei Med, 2025, 31(4): 543-549.
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2025, Vol. 31 
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