{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T02:04:54Z","timestamp":1791165894010,"version":"4.1.0"},"reference-count":60,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T00:00:00Z","timestamp":1765497600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"State assignment","award":["075-00607-25-00"],"award-info":[{"award-number":["075-00607-25-00"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biomolecules"],"abstract":"<jats:p>This study explores the effects of exogenous SELENOV on cellular migration, viability, mitochondrial function, ROS production, and Ca2+ signaling in mouse fibroblast L-929 and testicular teratoma F-9 cells. In scratch assays, 50\u2013100 \u00b5g\/mL SELENOV significantly inhibited F-9 cell migration after 48 h, while in L-929 fibroblasts, only 100 \u00b5g\/mL had a suppressive effect. Viability assays revealed strong cytotoxicity in F-9 cells. Critically, at a dose of 50 \u00b5g\/mL (where the corresponding volume of solvent buffer alone was non-toxic), SELENOV reduced survival to 19%, triggering late apoptosis in 76% of cells, whereas in L-929 cells, comparable effects required 100 \u00b5g\/mL. Mitochondrial depolarization (JC-1\/Rhodamine-123 assays) was pronounced in F-9 cells even at 50 \u00b5g\/mL, while L-929 cells responded only to 100 \u00b5g\/mL. Similarly, 50 \u00b5g\/mL SELENOV induced significant ROS overproduction in F-9 but not in L-929 cells, correlating with upregulated NOX1, NOX4, GPX3, and GPX4 expression. Ca2+ imaging showed dose-dependent [Ca2+]\u1d62 elevation, with 50 \u00b5g\/mL SELENOV inducing a sustained rise in F-9 cells, whereas L-929 cells required higher doses. Strikingly, 50 \u00b5g\/mL SELENOV in F-9 cells downregulated BCL-2 and BCL-xL while upregulating pro-apoptotic BAX and PUMA, suggesting selective activation of intrinsic apoptosis. These results demonstrate that F-9 cancer cells are significantly more sensitive to SELENOV than normal fibroblasts, with 50 \u00b5g\/mL sufficient to trigger mitochondrial dysfunction, oxidative stress, and apoptosis. The findings highlight SELENOV\u2019s potential as a targeted anticancer agent, particularly for germ cell tumors.<\/jats:p>","DOI":"10.3390\/biom15121733","type":"journal-article","created":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T15:27:20Z","timestamp":1765553240000},"page":"1733","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Exogenous Selenoprotein V Induces Apoptosis in Murine Testicular Teratoma Cells via Mitochondrial Dysfunction and ROS Overproduction"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2528-8798","authenticated-orcid":false,"given":"Egor A.","family":"Turovsky","sequence":"first","affiliation":[{"name":"Institute of Cell Biophysics of the Russian Academy of Sciences, Federal Research Center \u201cPushchino Scientific Center for Biological Research of the Russian Academy of Sciences\u201d, 142290 Pushchino, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1158-5174","authenticated-orcid":false,"given":"Elena G.","family":"Varlamova","sequence":"additional","affiliation":[{"name":"Institute of Cell Biophysics of the Russian Academy of Sciences, Federal Research Center \u201cPushchino Scientific Center for Biological Research of the Russian Academy of Sciences\u201d, 142290 Pushchino, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,12,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Mariotti, M., Ridge, P.G., Zhang, Y., Lobanov, A.V., Pringle, T.H., Guigo, R., Hatfield, D.L., and Gladyshev, V.N. 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