Analysis finds cardiac troponin I promotes cell proliferation in lung cancer, indicating its role in tumor growth mechanisms.
Lung cancer is one of the most prevalent cancers, with 80%-85% of cases being non-small cell lung cancer (NSCLC). This study investigated the effect of cardiac troponin I (cTnI) on NSCLC cells and its molecular mechanism. The overexpression and knockdown of cTnI were performed in NSCLC cells using lentivirus. Expression assays to analyse gene mRNA levels were performed using RT- PCR, and Western blot was used to detect the protein expression. Cell proliferation capacity was tested using MTT and colony formation assays, and a Transwell® assay was used to detect cell migration and invasion. The in vivo experiments were performed using xenografts in nude mice. cTnI expression was increased in NSCLC tissue and cells. The overexpression of cTnI in NSCLC cells promoted their development, and the knockdown of cTnI inhibited the proliferation and migration of lung cancer cells. Additionally, cTnI promoted the expression of Notch and Kras proteins in lung cancer cells. The xenograft experiments in nude mice yielded the same results. Cardiac troponin I affects the proliferation and migration of NSCLC cells by promoting the expression of Notch and Kras proteins, and the knockdown of cTnI significantly inhibits the growth and development of NSCLC cells.
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Wang et al. (2025) studied this question.
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