{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T10:15:20Z","timestamp":1788430520625,"version":"build-2803163510"},"reference-count":61,"publisher":"MDPI AG","issue":"17","license":[{"start":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T00:00:00Z","timestamp":1788393600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"FUSP-CEU UCH","award":["INDI25\/62"],"award-info":[{"award-number":["INDI25\/62"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Rnd3 is an atypical member of the Rho GTPase family whose activity is mainly regulated by expression, localization and protein stability rather than canonical GDP\/GTP cycling. In cancer, Rnd3 has been described both as a tumor suppressor and as a tumor-promoting factor, creating an apparent functional paradox. We propose that this paradox is resolved by a mechanistic invariant: Rnd3 exerts a conserved inhibition of RhoA\/ROCK1-dependent actomyosin contractility, whose phenotypic output is redirected by context-specific accessory effectors rather than reversed. In this review, we revisit this paradox by integrating evidence from mechanistic studies, tumor models and patient-associated datasets. We propose that Rnd3 should not be interpreted through a binary oncogene\/tumor-suppressor framework, but rather as a context-dependent regulator of tumor cell state. In many tumor settings, Rnd3 repression or loss of Rnd3 function favors proliferation, apoptosis resistance and therapy resistance through pathways involving Notch, NF-\u03baB, EGFR\/ERK, EZH2-dependent chromatin regulation, m6A-mediated RNA control, microRNAs and chaperone-mediated autophagy. However, in selected contexts, including RTK-driven glioblastoma, hepatocellular carcinoma, non-small-cell lung cancer, melanoma and gastric cancer, Rnd3 may support tumor fitness, migration or invasive plasticity. We therefore propose a functional stratification model in which Rnd3 output depends on the biological process, tumor lineage, pathway activity and mechanical state of the cell.<\/jats:p>","DOI":"10.3390\/cells15171602","type":"journal-article","created":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T09:20:43Z","timestamp":1788427243000},"page":"1602","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Context-Dependent Roles of Rnd3 in Cancer: Revisiting a Functional Paradox"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7616-1818","authenticated-orcid":false,"given":"Elisa","family":"Lled\u00f3","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, School of Health Sciences, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olga","family":"G\u00f3mez","sequence":"additional","affiliation":[{"name":"Department of Animal Medicine and Surgery, Facultad de Veterinaria, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra","family":"Bizy","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, School of Health Sciences, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amalia","family":"Solana-Orts","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, School of Health Sciences, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7356-2341","authenticated-orcid":false,"given":"Jos\u00e9","family":"Terrado","sequence":"additional","affiliation":[{"name":"Department of Animal Medicine and Surgery, Facultad de Veterinaria, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7413-9334","authenticated-orcid":false,"given":"Bego\u00f1a","family":"Ballester-Lurbe","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, School of Health Sciences, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9416-8047","authenticated-orcid":false,"given":"Enric","family":"Poch","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, School of Health Sciences, Universidad Cardenal Herrera-CEU, CEU Universities, 46115 Alfara del Patriarca, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,9,3]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Clayton, N.S., and Ridley, A.J. 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