{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T21:37:03Z","timestamp":1793914623684,"version":"4.8.0"},"reference-count":92,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"644","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2022,5,11]]},"abstract":"<jats:p>\n            Despite the hyperproliferative environment marked by activation of \u03b2-catenin and overexpression of\n            <jats:italic>c-myc<\/jats:italic>\n            , the epidermis surrounding chronic diabetic foot ulcers (DFUs) is clinically hypertrophic and nonmigratory yet does not undergo malignant transformation. We identified miR193b-3p as a master regulator that contributes to this unique cellular phenotype. We determined that induction of tumor suppressor miR193b-3p is a unique feature of DFUs that is not found in venous leg ulcers, acute wounds, or cutaneous squamous cell carcinoma (SCC). Genomic analyses of DFUs identified suppression of the miR193b-3p target gene network that orchestrates cell motility. Inhibition of migration and wound closure was further confirmed by overexpression of miR193b-3p in human organotypic and murine in vivo wound models, whereas miR193b-3p knockdown accelerated wound reepithelialization in human ex vivo and diabetic murine wounds in vivo. The dominant negative effect of miR193b-3p on keratinocyte migration was maintained in the presence of promigratory miR31-5p and miR15b-5p, which were also overexpressed in DFUs. miR193b-3p mediated antimigratory activity by disrupting stress fiber formation and by decreasing activity of GTPase RhoA. Conversely, miR193b-3p targets that typically participate in malignant transformation were found to be differentially regulated between DFUs and SCC, including the proto-oncogenes\n            <jats:italic>KRAS<\/jats:italic>\n            (Kirsten rat sarcoma viral proto-oncogene) and\n            <jats:italic>KIT<\/jats:italic>\n            (KIT proto-oncogene). Although miR193b-3p acts as a tumor suppressor contributing to low tumor incidence in DFUs, it also acts as a master inhibitor of cellular migration and epithelialization in DFUs. Thus, miR193b-3p may represent a target for wound healing induction, cancer therapeutics, and diagnostics.\n          <\/jats:p>","DOI":"10.1126\/scitranslmed.abg8397","type":"journal-article","created":{"date-parts":[[2022,5,11]],"date-time":"2022-05-11T17:54:30Z","timestamp":1652291670000},"source":"Crossref","is-referenced-by-count":25,"title":["Dichotomous role of miR193b-3p in diabetic foot ulcers maintains inhibition of healing and suppression of tumor formation"],"prefix":"10.1126","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2770-3083","authenticated-orcid":true,"given":"Jelena","family":"Marjanovic","sequence":"first","affiliation":[{"name":"Wound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, 33136, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Horacio 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