By: Shuang Fu, Likun Liu, Yaoyao Wang, Wenlu Liu, Siyu Sun, Xiu li Gao, Wenbin Zhu, Liling Yue
Keywords: Hydroxychloroquine; A549 cell; antitumor action; G1 phase arrest; apoptosis.
DOI : 10.36721/PJPS.2024.37.5.REG.981-991.1
Abstract: Hydroxychloroquine, used initially as an anti-malarial drug, is now recognized for its anti-tumor effects in a range of human cancers. Nevertheless, there has been limited attention given to the molecular mechanisms of anti-tumor action of hydroxychloroquine. Here, we investigated the anti-tumor effect of hydroxychloroquine in human A549 cells and further analyzed the potential molecular mechanisms involved. Hydroxychloroquine was found to effectively inhibit the growth of A549 cells. This inhibition was observed to be both dose-dependent and time-dependent. Moreover, in a tumor xenograft mouse model, hydroxychloroquine remarkably suppressed tumor growth. Mechanistically, treatment with hydroxychloroquine led to the inhibition of phosphorylation in JNK, STAT3 and AKT. This biochemical interference subsequently induced G1 cell cycle arrest and promoted mitochondrial-mediated apoptosis in A549 cells. The findings from this study offered robust evidence supporting the use of hydroxychloroquine as a treatment for non-small cell lung cancer (NSCLC). Consequently, hydroxychloroquine emerges as a potential therapeutic agent for the treatment of this cancer.
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