BAP18 induces growth of non-small-cell lung carcinoma through upregulating transcriptional level of CCND1/2

• Published in: European review for medical and pharmacological sciences Vol. 26; no. 9; p. 3074
• Main Authors: Wei, S-J, Li, J, Wang, J-Y, Zhang, L-X, Zhang, H-B, Du, D-J, Li, Q-X
• Format: Journal Article
• Language: English
• Published: Italy 01.05.2022
• Subjects: Carcinoma, Non-Small-Cell Lung - pathology; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Cyclin D1 - genetics; Cyclin D1 - metabolism; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms - pathology; MicroRNAs
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_202205_28724

To elucidate the biological function of BAP18 (BPTF-associated protein of 18 kDa) in non-small-cell lung carcinoma (NSCLC) and the molecular mechanism. Relative levels of BAP18 in NSCLC tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and its influence on pathological characteristics of NSCLC patients was analyzed. Correlation between BAP18 and Ki67 levels in NSCLC was assessed by Pearson correlation test. Furthermore, Kaplan-Meier curves were depicted for revealing survival difference in NSCLC patients expressing high or low level of BAP18. Relative levels of BAP18, CCND1, CCND2 and CCND3 in A549 and H1299 cells transfected with siBAP18 were determined, as well as colony number. In addition, after knockdown of protein level of BAP18 in A549 and H1299 cells by lentivirus transfection, cell cycle progression was examined. Co-regulation of BAP18 and CCND1/2 on cell growth of NSCLC was finally detected. BAP18 was upregulated in NSCLC tissues, especially cases with advanced stage (III-IV) or large tumor size (>5 cm). BAP18 was closely linked to tumor size, TNM staging and lymphatic metastasis in NSCLC. Knockdown of BAP18 reduced transcriptional levels of CCND1 and CCND2 in A549 and H1299 cells. Furthermore, knockdown of BAP18 delayed transition from G1 to S phase, and weakened growth of NSCLC cells. BAP18 triggers the progression of NSCLC by regulating transcriptional activities of CCND1/2, which may be a potential target for the treatment and diagnosis of NSCLC.