{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T12:14:05Z","timestamp":1780402445119,"version":"3.54.1"},"reference-count":58,"publisher":"Public Library of Science (PLoS)","issue":"4","license":[{"start":{"date-parts":[[2023,4,21]],"date-time":"2023-04-21T00:00:00Z","timestamp":1682035200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National science and technology council, Taiwan","award":["108-2314-B-007-003-MY3"],"award-info":[{"award-number":["108-2314-B-007-003-MY3"]}]},{"name":"National Science and Technology Council, Taiwan","award":["111-2320-B-007-005-MY3"],"award-info":[{"award-number":["111-2320-B-007-005-MY3"]}]},{"DOI":"10.13039\/501100005057","name":"National Tsing Hua University","doi-asserted-by":"publisher","award":["112Q2511E1"],"award-info":[{"award-number":["112Q2511E1"]}],"id":[{"id":"10.13039\/501100005057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005057","name":"National Tsing Hua University","doi-asserted-by":"publisher","award":["111Q2713E1"],"award-info":[{"award-number":["111Q2713E1"]}],"id":[{"id":"10.13039\/501100005057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005057","name":"National Tsing Hua University","doi-asserted-by":"publisher","award":["112Q2521E1"],"award-info":[{"award-number":["112Q2521E1"]}],"id":[{"id":"10.13039\/501100005057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:p><jats:italic>RAS<\/jats:italic>, the most frequently mutated oncogene that drives tumorigenesis by promoting cell proliferation, survival, and motility, has been perceived as undruggable for the past three decades. However, intense research in the past has mainly focused on<jats:italic>KRAS<\/jats:italic>mutations, and targeted therapy for<jats:italic>NRAS<\/jats:italic>mutations remains an unmet medical need.<jats:italic>NRAS<\/jats:italic>mutation is frequently observed in several cancer types, including melanoma (15\u201320%), leukemia (10%), and occasionally other cancer types. Here, we report using miRNA-708, which targets the distinct 3\u2019 untranslated region (3\u2019UTR) of<jats:italic>NRAS<\/jats:italic>, to develop miRNA-based precision medicine to treat<jats:italic>NRAS<\/jats:italic>mutation-driven cancers. We first confirmed that<jats:italic>NRAS<\/jats:italic>is a direct target of miRNA-708. Overexpression of miRNA-708 successfully reduced NRAS protein levels in melanoma, leukemia, and lung cancer cell lines with<jats:italic>NRAS<\/jats:italic>mutations, resulting in suppressed cell proliferation, anchorage-independent growth, and promotion of reactive oxygen species-induced apoptosis. Consistent with the functional data, the activities of NRAS-downstream effectors, the PI3K-AKT-mTOR or RAF-MEK-ERK signaling pathway, were impaired in miR-708 overexpressing cells. On the other hand, cell proliferation was not disturbed by miRNA-708 in cell lines carrying wild-type<jats:italic>NRAS<\/jats:italic>. Collectively, our data unveil the therapeutic potential of using miRNA-708 in<jats:italic>NRAS<\/jats:italic>mutation-driven cancers through direct depletion of constitutively active NRAS and thus inhibition of its downstream effectors to decelerate cancer progression. Harnessing the beneficial effects of miR-708 may therefore offer a potential avenue for small RNA-mediated precision medicine in cancer treatment.<\/jats:p>","DOI":"10.1371\/journal.pone.0284744","type":"journal-article","created":{"date-parts":[[2023,4,21]],"date-time":"2023-04-21T17:27:36Z","timestamp":1682098056000},"page":"e0284744","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":9,"title":["MicroRNA-708 emerges as a potential candidate to target undruggable NRAS"],"prefix":"10.1371","volume":"18","author":[{"given":"Jia Meng","family":"Pang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Po-Chen","family":"Chien","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming-Chien","family":"Kao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei-Yun","family":"Chiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pin-Xu","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu-Ling","family":"Hsu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengyang","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaowei","family":"Liang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8656-5755","authenticated-orcid":true,"given":"Kai-Ti","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2023,4,21]]},"reference":[{"issue":"1","key":"pone.0284744.ref001","doi-asserted-by":"crossref","first-page":"17","DOI":"10.1016\/j.cell.2017.06.009","article-title":"RAS 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