Key points are not available for this paper at this time.
Abstract Nicotine is a psychoactive component of cigarette smoke responsible for addictive properties of tobacco and is shown to promote cancer pathogenesis. We earlier reported that exosomes released from nicotine-treated prostate cancer cells played a key role in tumor angiogenesis, a process necessary to maintain the supply of nutrients and oxygen to the fast proliferating cancer cells. Here, we examined the molecular mechanisms underlying the exosome-mediated effect of nicotine on angiogenesis. For this, we screened the expression of angiogenesis-related miRNAs in the exosomes derived from LNCaP and C4-2 cells treated with vehicle or nicotine (400 nM). Highest and most differential abundance of miR-3157-3p was found in exosomes derived from nicotine-treated prostate cancer cells. Furthermore, the expression of TIMP-2 and KLF-2, established targets of miR-3157-3p, was also downregulated in endothelial cells transfected with exosomes derived from nicotine-treated prostate cancer cells or miR-3157-3p mimics. Studies are currently underway to establish direct targeting of TIMP-2 and KLF-2 by miR-3157-3p and confirm that their suppression is indeed associated with observed changes in endothelial cell growth, migration and capillary-forming ability. Citation Format: Shubhangi Singh, Mohammad Aslam Khan, Shashi Anand, Sirin Saranyutanon, Sanjeev Kumar Srivastava, Seema Singh, Ajay P. Singh, Kunwar Somesh Vikramdeo. Nicotine-induced exosomal miR-3157-3p from prostate cancer cells promotes angiogenesis abstract. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts) ; 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84 (6Suppl): Abstract nr 5394.
Singh et al. (Fri,) studied this question.