LINC01614促进肺鳞状细胞癌细胞增殖及进展的致病机制研究

doi:10.3969/j.issn.1006-6233.2025.04.03

Abstract
Figure/Table
References
Related Citation (15)

Download: PDF (2511 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

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.

Key words： Lung squamous cell carcinoma LINC01614 PI3K/Akt Cancer cell proliferation

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors

Cite this article:

URL:

http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2025.04.03 OR http://www.hbyxzzs.cn/EN/Y2025/V31/I4/543

[1] Sung H,Ferlay J,Siegel RL,et al.Global cancer statistics 2020:GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J].CA Cancer Clin,2021,71(3):209-249.
[2] Herbst RS,Morgensztern D,Boshoff C.The biology and management of non-small cell lung cancer[J].Nature,2018,553(7689):446-454.
[3] 郭丽娜,王宏伟.联合免疫检查点抑制剂治疗驱动基因阴性非小细胞肺癌脑转移的研究进展[J].中国肿瘤临床,2024,51(3):153-158.
[4] 刘传,李琦.肺鳞状细胞癌靶向治疗研究进展[J].肿瘤,2024,44(1):25-33.
[5] Yuan H,Liu J,Zhang J.The current landscape of immune checkpoint blockade in metastatic lung squamous cell carcinoma[J].Molecules,2021,6(5):1392.
[6] Sun Y,Ling C.Analysis of the long non-coding RNA LINC01614 in non-small cell lung cancer[J].Medicine (Baltimore),2019,98(30):16437.
[7] Niu Z,Jin R,Zhang Y,et al.Signaling pathways and targeted therapies in lung squamous cell carcinoma:mechanisms and clinical trials[J].Signal Transduct Target Ther,2022,7(1):353.
[8] Mao G,Mu Z,Wu DA.Exosomal LncRNA FOXD3-AS1 upregulates ELAVL1 expression and activates PI3K/Akt pathway to enhance lung cancer cell proliferation,invasion,and 5-fluorouracil resistance[J].Acta Biochim Biophys Sin (Shanghai),2021,53(11):1484-1494.
[9] Yan S,Xu J,Liu B,et al.Integrative bioinformatics analysis identifies LINC01614 as a potential prognostic signature in esophageal cancer[J].Transl Cancer Res,2021,10(4):1804-1812.
[10] Li W,Cheng Y,Cheng J,et al.Long noncoding RNA LINC01614 is a diagnostic and prognostic marker for breast cancer[J].Discov Med,2023,35(174):19-27.
[11] Hou Y,Zhou M,Li Y,et al.Risk SNP-mediated LINC01614 upregulation drives head and neck squamous cell carcinoma progression via PI3K/AKT signaling pathway[J].Mol Carcinog,2022,61(8):797-811.
[12] Chen T,Shi K,Sun S.LINC01614 activated by SP1 promoted malignant behavior of triple-negative breast cancer cells via the WNT/b-Catenin signaling pathway[J].Rev Invest Clin,2024,76(4):185-194.