A potential anticancer effect of a new molecule named 4g on lung cancer cell line H292

P53 directs the cellular response to stress, leading to cell cycle arrest, senescence or apoptosis. IL6 and IL8, increased in lung cancer, cause the loss of p53 in normal cells and promote epithelial mesenchymal transition, a crucial mechanism in cancer metastasis. The interaction between oncogenic signaling and metabolic pathways could lead to new therapeutic strategies in lung cancer. A new promising anticancer molecule named 4g, a pyrrolo[3,2-c]quinoline scaffold in which, an insertion of a 4-benzo[d][1,3]dioxol-5-yl moiety, exerted anti-proliferative and pro-apototic effects in a breast cancer cell line (MCF7). The anticancer effects of 4g in lung cancer are largely unknown. Aim: the present study was assessed to investigate the effects of 4g on a lung cancer cell line (H292), evaluating p53 expression, cell proliferation and IL8 and IL6 release. Method: we treated H292 cells with 4g at 5, 10 and 25μM. We evaluated nuclear and cytoplasmic p53 expression by western blotting. Cell proliferation was assed by clonogenic assay. Cell metabolism and viability was evaluated by MTS. IL8 and IL6 release was detected by ELISA. Results: 4g increased both nuclear and cytoplasmic p53 expression, reduced long term cell proliferation, altered cell metabolism affecting cell viability and decreased IL6 and IL8 release. Conclusion: These results suggest, for the first time, that 4g molecule carries out its anti-lung cancer activity, increasing nuclear p53, that in turn could reduce cell proliferation and downregulate the secretory milieu that fuel cancer growth, progression, metastasis, and recurrence