Ученые доказали, что пар от электронных сигарет запускает процессы, ведущие к раку легких

By: Eunice Jean C. Patron Scientists from the University of the Philippines Diliman (UPD) provided new evidence on the tumorigenic effects of vaping, helping to throw light on recent reports that show e-cigarette smoke can significantly alter the transcriptome of respiratory epithelia. Daniel Angelo Mirador, Jose Lorenzo Ferrer, Kim Denyse Hao Lin, and Dr. Reynaldo Garcia of the UPD College of Science’s National Institute of Molecular Biology and Biotechnology (UPD-CS NIMBB) investigated how vape use may affect cancer-related cellular processes. They focused on a molecule they named vape-associated lncRNA transcript 1 (VALT1), which was found to be elevated in vape users and in certain lung cancer tumors, and examined how it behaves in human cells exposed to e-cigarette vapor. “In an earlier study that we published in Scientific Reports, we reported that the long noncoding RNA called smoke- and cancer-associated lncRNA transcript 1 (SCAL1) ensures the survival of cancer cells whose DNA has been damaged by cigarette smoke. It does so by detoxifying cells of reactive oxygen species (ROS) that would otherwise lead to cell death. This creates a paradox: instead of dying, the damaged cells persist, which can promote cancer development—creating a kind of double jeopardy,” Dr. Garcia explained. “The motivation for this study was to ask whether a similar mechanism also occurs with vaping: can vape exposure trigger changes in cells that, like cigarette smoke, allow damaged cells to survive?” The team of molecular biologists demonstrated that exposure to vape chemicals increases VALT1 levels and concomitantly enhance cell proliferation, resistance to programmed cell death, cell migration, ROS detoxification, cytoskeletal disorganization, and nuclear remodeling—the same hallmarks observed in tumorigenic cells. Interestingly, VALT1 overexpression can have these effects even without vape exposure. Moreover, VALT1 can promote survival of cells under cytotoxic stress, such as the lung cancer cell line A549, but not its normal counterpart. “This provides evidence that vaping is not safe, and that its harmful effects are mediated, at least partly, by VALT1. Our cells assume tumorigenic properties upon exposure to e-cigarettes,” Mirador said. “Beyond its health implications, this work also contributes to our knowledge of non-coding RNA biology. The study of non-coding RNAs is relatively recent. They were initially dismissed as junk but are now established to have roles in both normal cell physiology and disease pathogenesis.” While e-cigarettes may have a lower chemical load, they have been implicated in severe respiratory illnesses and cardiovascular damage. The team noted that it may take decades to fully understand the long-term effects of e-cigarettes, including whether they contribute to cancer. Lung oncogenesis has a long induction and latency period while vaping has not been around for a long period of time. Studies on the effects of vaping at the cellular and molecular level also remain limited, highlighting the need for further investigations to build a stronger scientific foundation. Their research, “Vape-Associated lncRNA Transcript 1 (VALT1) Amplifies the Tumorigenic Effects of e-Cigarette Vapor in Lung Epithelial Cells,” is published in Non-Coding RNA, an international, peer-reviewed, open access journal on non-coding RNA research dealing with elucidating the structure, function and biology of regulatory non-coding RNAs. For interview requests and other concerns, please contact [email protected]. References: Mirador, D. A., Ferrer, J. L., Lin, K. D., & Garcia, R. L. (2026). Vape-associated lncRNA transcript 1 (VALT1) amplifies the tumorigenic effects of e-cigarette vapor in lung epithelial cells. Non-Coding RNA, 12(2), 10. https://doi.org/10.3390/ncrna12020010