{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T11:31:16Z","timestamp":1781177476969,"version":"3.54.1"},"reference-count":26,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2021,1,18]],"date-time":"2021-01-18T00:00:00Z","timestamp":1610928000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Photoderm Photoimm Photomed"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Chronic actinic dermatitis (CAD) is a photoallergic skin disease with abnormal hyperplasia. At present, the mechanism of abnormal proliferation is not clear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To explore possible mechanism of CAD proliferative lesions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Immunohistochemistry (IHC) assay and small RNA sequencing were carried out. Quantitative real\u2010time PCR (qRT\u2010PCR) analysis was performed to evaluate expression levels of hsa\u2010miR\u2010221\u20103p and FOS. The interaction between hsa\u2010miR\u2010221\u20103p and FOS was identified by dual\u2010luciferase reporter assay. Expression of hsa\u2010miR\u2010221\u20103p also was detected by qRT\u2010PCR after UVB irradiation. Influences of hsa\u2010miR\u2010221\u20103p and FOS on cell viability and apoptosis were assessed through a series of functional experiments and rescue experiments. Western blot analysis was used to detect protein expression of fos, Bax, Bcl\u2010xL, and caspase\u20103.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Patients with CAD had marked epidermal hyperplasia. The expression of hsa\u2010miR\u2010221\u20103p was up\u2010regulated in CAD while FOS was significantly down\u2010regulated. Dual\u2010luciferase reporter assay confirmed that hsa\u2010miR\u2010221\u20103p targeted FOS 3'UTR. Hsa\u2010miR\u2010221\u20103p induced by UVB ranged from 0 to 30\u00a0mJ. Moreover, hsa\u2010miR\u2010221\u20103p overexpression or FOS knockdown promoted cell proliferation and reduced cell apoptosis. Western blot showed that hsa\u2010miR\u2010221\u20103p negatively regulated fos, which regulated Bcl\u2010xL\/Bax. Cell proliferation caused by hsa\u2010miR\u2010221\u20103p overexpression or FOS knockdown could be reversed by Bcl\u2010xL inhibitor.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Hsa\u2010miR\u2010221\u20103p induced by UVB targeted FOS 3\u2032UTR, which played an important role in regulating proliferation and apoptosis of keratinocytes via Bcl\u2010xL\/Bax pathway; this may provide a new insight for CAD proliferative lesions.<\/jats:p><\/jats:sec>","DOI":"10.1111\/phpp.12647","type":"journal-article","created":{"date-parts":[[2020,12,23]],"date-time":"2020-12-23T06:01:41Z","timestamp":1608703301000},"page":"269-277","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Up\u2010regulation of hsa\u2010miR\u2010221\u20103p induced by UVB affects proliferation and apoptosis of keratinocytes via Bcl\u2010xL\/Bax 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