{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T01:50:24Z","timestamp":1760061024864,"version":"build-2065373602"},"reference-count":61,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2020,4,23]],"date-time":"2020-04-23T00:00:00Z","timestamp":1587600000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:sec><jats:label\/><jats:p>Growing data have recognized the significance of Response Gene to Complement (RGC)\u201032 in numerous tumour developments. Notwithstanding, the functional role and underlying mechanism of it in tongue squamous cell carcinoma (TSCC) remain enigmatic. Here, to identify the impact of RGC\u201032 in TSCC, its expression in multiple TSCC cells was measured and loss\u2010of\u2010function experiments in cell lines were performed to illuminate the function of it induced TSCC progression, via si\u2010RNA knockdown, CCK\u20108, colony formation, wound\u2010healing, transwell, flow cytometry and western blot assays. To clarify potential mechanism, expressions of hallmarks in epithelial\u2010mesenchymal transition (EMT) process and PI3K\/AKT signalling were assessed, and the upstream miR regulator of RGC\u201032 was predicted and verified by applying bioinformatic approaches and dual\u2010luciferase reporter assay, respectively. Finally, the rescue experiments were applied to better elucidate the effect of miR\u201026b\/RGC\u201032 axis in TSCC behaviours. As a result, RGC\u201032 was upregulated in TSCC cells and knocking down of it abrogated cell proliferation, trans\u2010migration and invasion, whilst promoted apoptosis in TSCC, which was regulated through repressing EMT and inactivation of PI3K\/AKT signalling. Subsequently, miR\u201026b was predicted and identified as an upstream regulator of RGC\u201032, and the pro\u2010tumorigenic effect of RGC\u201032 was reversed by miR\u201026b overexpression. Collectively, our results demonstrated that RGC\u201032 facilitated TSCC progression, which was modulated by activations of PI3K\/AKT pathway and EMT process, and reduction of its negative regulator of miR\u201026b. These findings highlight a novel role of miR\u201026b\/RGC\u201032 axis in TSCC and underlying mechanism, encouraging a potent usage in TSCC treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance of the study<\/jats:title><jats:p>We first uncovered that Response Gene to Complement\u201032 played a significantly pro\u2010tumorigenic role in tongue squamous cell carcinoma (TSCC), which was closely regulated by downregulation of miR\u201026b and activations of epithelial\u2010mesenchymal transition process and PI3K\/AKT signalling. These findings contribute to better understand the molecular mechanism in carcinogenesis of TSCC, and shed some light on promising strategy for TSCC therapeutics.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbf.3520","type":"journal-article","created":{"date-parts":[[2020,4,23]],"date-time":"2020-04-23T18:55:10Z","timestamp":1587668110000},"page":"943-954","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Oncogenic gene RGC\u201032 is a direct target of miR\u201026b and facilitates tongue squamous cell carcinoma aggressiveness through EMT and PI3K\/AKT signalling"],"prefix":"10.1002","volume":"38","author":[{"given":"Zhong\u2010Heng","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Stomatology The First Affiliated Hospital of Jinzhou Medical University  Jinzhou Liaoning 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