{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T12:36:14Z","timestamp":1762432574593,"version":"3.41.2"},"reference-count":37,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2025,7,16]],"date-time":"2025-07-16T00:00:00Z","timestamp":1752624000000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100009330","name":"Medical Science and Technology Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["A2022147"],"award-info":[{"award-number":["A2022147"]}],"id":[{"id":"10.13039\/501100009330","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Psoriasis is a chronic autoimmune skin disease characterised by a high recurrence rate and epidermal hyperproliferation. Recent studies have highlighted the pathogenic roles of long non\u2010coding RNAs (lncRNAs) in psoriasis. However, the cellular functions and underlying mechanisms of most lncRNAs remain largely unknown. In this study, we identified functional lncRNAs associated with cell cycle regulation through integrative analysis of RNA\u2010seq datasets from a psoriasis cohort. Interestingly, we observed significant upregulation of <jats:italic>LINC01206<\/jats:italic> in skin biopsies from psoriatic lesions, whereas its expression was downregulated following glucocorticoid treatment. Furthermore, we constructed a lncRNA\u2010protein\u2010coding gene (PCG) co\u2010expression network, which revealed that <jats:italic>LINC01206<\/jats:italic> tends to co\u2010express with cell cycle\u2010related genes, such as <jats:italic>CCNB1<\/jats:italic> and <jats:italic>CCNE1.<\/jats:italic> Using an in\u00a0vitro keratinocyte model, we demonstrated that LINC01206 disrupts cell cycle progression, and its knockdown induced cell cycle arrest at the G0\/G1 phase. Additional functional experiments showed that the expression of hyperproliferation\u2010associated keratins decreased upon <jats:italic>LINC01206<\/jats:italic> knockdown. Mechanistically, <jats:italic>LINC01206<\/jats:italic> promotes cell cycle progression at the G0\/G1 phase by modulating the activity of Ets homologous factor (EHF). Our findings suggest that <jats:italic>LINC01206<\/jats:italic> enhances keratinocyte proliferation in psoriasis by regulating cell cycle progression, making it a potential therapeutic target for psoriasis treatment.<\/jats:p>","DOI":"10.1111\/jcmm.70719","type":"journal-article","created":{"date-parts":[[2025,7,17]],"date-time":"2025-07-17T03:10:26Z","timestamp":1752721826000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["<scp>LncRNA LINC01026<\/scp> Is Overexpressed in Psoriasis and Enhances Keratinocyte Cell Cycle Progression by Regulating the Ets Homologous Factor (<scp>EHF<\/scp>)"],"prefix":"10.1111","volume":"29","author":[{"given":"Jingxia","family":"Lin","sequence":"first","affiliation":[{"name":"Dermatology Hospital Southern Medical University  Guangzhou Guangdong China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hang","family":"Su","sequence":"additional","affiliation":[{"name":"Dermatology Hospital Southern Medical University  Guangzhou Guangdong China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuanqiu","family":"Zhong","sequence":"additional","affiliation":[{"name":"Dermatology Hospital Southern Medical University  Guangzhou Guangdong China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hang","family":"Zheng","sequence":"additional","affiliation":[{"name":"Dermatology Hospital Southern Medical University  Guangzhou Guangdong China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yongfeng","family":"Chen","sequence":"additional","affiliation":[{"name":"Dermatology Hospital Southern Medical University  Guangzhou Guangdong China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2025,7,16]]},"reference":[{"key":"e_1_2_9_2_1","first-page":"E6162","article-title":"Keratinocytes Contribute Intrinsically to Psoriasis Upon Loss of Tnip1 Function","volume":"113","author":"Ippagunta S. 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