Affiliations: [a] Department of Thoracardiac Surgery, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China | [b] Department of Thoracic surgery, Ya’an City Second People’s Hospital, Ya’an, Sichuan, China
Correspondence:
[*]
Corresponding author: Zhiqiang Wu, Department of Thoracardiac Surgery, The First Affiliated Hospital of Chengdu Medical College, No. 278, Middle Section of Baoguang Avenue, Xindu District, Chengdu, Sichuan 610500, China. Tel./Fax: +86 19138983721; E-mail: [email protected].
Note: [1] These authors contributed equally to this study.
Abstract: BACKGROUND: It has been discovered that lncRNA ARAP1-AS1 is upregulated and operates as a tumor promoter in many cancers. However, its pattern of expression and potential mechanism in lung adenocarcinoma (LUAD) is still unknown. METHODS: The levels of lncRNA ARAP1-AS1, miR-8068, and CEACAM5 expressions in LUAD cell lines and tissues were assessed by conducting western blot and RT-qPCR analyses. MiR-8068’s potential targeting relationships with lncRNA ARAP1-AS1 and CEACAM5 were ascertained by performing bioinformatics analysis. The interaction of lncRNA ARAP1-AS1 with miR-8068 was validated by means of by RIP and luciferase reporter experiments. CCK-8, cell adhesion, and Transwell migration experiments were conducted to study how lncRNA ARAP1-AS1 affects LUAD cell migration, adhesion, and proliferation. To confirm the function of lncRNA ARAP1-AS1 in vivo, a tumor formation experiment was executed. RESULTS: An elevated expression of lncRNA ARAP1-AS1 was observed among the LUAD cells and tissues. The overexpression of lncRNA ARAP1-AS boosted cell proliferation, adhesion, and migration in LUAD and also favored in vivo tumor growth. MiR-8068 was found to be lncRNA ARAP1-AS1’s target gene. MiR-8068 overexpression partially antagonized lncRNA ARAP1-AS1’s promotive effect on proliferation, viability, and adhesion. Meanwhile CEACAM5 could alleviate the miR-8068-induced inhibition of tumor growth. The negative correlation of miR-8068 with lncRNA ARAP1-AS1 or CEACAM5 was also revealed. CONCLUSION: To upregulate CEACAM5 expression lncRNA ARAP1-AS1 targeted miR-8068, thus promoting the progression of LUAD. This indicates that the lncRNA ARAP1-AS1/miR-8068/CEACAM5 axis has potential as a therapeutic target in LUAD treatment.
