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近日，國(guó)際著名學(xué)術(shù)期刊Journal of the American Chemical Society（IF 14.695）在線(xiàn)發(fā)表了中國(guó)藥科大學(xué)生命科學(xué)與技術(shù)學(xué)院徐寒梅教授團(tuán)隊(duì)的最新研究成果“Micropeptide MIAC Inhibits HNSCC Progression by Interacting with Aquaporin 2”。課題組成員博士后李夢(mèng)瑋和碩士生李鑫為論文的共同第一作者，徐寒梅教授為通訊作者，中國(guó)藥科大學(xué)為第一作者單位和第一通訊單位。江蘇省口腔醫(yī)院武和明主任和丁旭醫(yī)生對(duì)本論文亦有重要貢獻(xiàn)。

近年科學(xué)家研究發(fā)現(xiàn)長(zhǎng)鏈非編碼RNA (long non coding RNA, lncRNAs，lncRNA）實(shí)際包含能編碼微肽 (micropeptides)的小開(kāi)放閱讀框 (sORF)，這為蛋白質(zhì)組學(xué)研究提供了一個(gè)新的視角。目前已發(fā)現(xiàn)的由lncRNA編碼的微肽報(bào)道并不多。本研究首次在頭頸鱗癌中發(fā)現(xiàn)由lncRNA AC025154.2編碼的全新內(nèi)源性微肽MIAC，體內(nèi)外實(shí)驗(yàn)發(fā)現(xiàn)MIAC能抑制頭頸鱗癌的增殖和轉(zhuǎn)移，蛋白質(zhì)譜和酵母雙雜交結(jié)果顯示MIAC能結(jié)合水通道蛋白，通過(guò)調(diào)控Sept2/ITGB4表達(dá)抑制骨架蛋白重排，最終抑制頭頸鱗癌進(jìn)展。結(jié)合500例TCGA數(shù)據(jù)庫(kù)頭頸鱗癌RNA-seq數(shù)據(jù)和154例臨床樣本檢測(cè)分析證實(shí)MIAC在頭頸鱗癌組織中表達(dá)顯著低于癌旁組織，其表達(dá)水平與患者總生存率呈正相關(guān)，與臨床病理分期，區(qū)域淋巴結(jié)轉(zhuǎn)移呈負(fù)相關(guān)，提示MIAC可以作為頭頸鱗癌臨床診斷和預(yù)后的潛在標(biāo)志物。

同時(shí)，課題組成員博士后王穎和碩士生陸繼強(qiáng)為共同第一作者，徐寒梅教授為通訊作者在Molecular Therapy-Nucleic Acids（IF 5.919）雜志上發(fā)表了小RNA分子的最新研究。研究圍繞著食管癌細(xì)胞來(lái)源的外泌體miR-181b-5p展開(kāi)，解析了其調(diào)控腫瘤血管生成的分子機(jī)制，有望為食管癌患者的臨床診治和預(yù)后評(píng)估提供新型的生物標(biāo)記分子和潛在的藥物靶點(diǎn)。

此外，近三年徐寒梅教授團(tuán)隊(duì)在RNA與腫瘤關(guān)系的其它研究成果還發(fā)表于Clin Cancer Res (Lin C, Zhang S, Xu H*.2018 Jan 15;24(2):486-498, IF 8.911)，Oncogene (Lin C, Wang Y, Xu H*. 2017 Sep 21;36(38):5392-5406, IF 6.854)，Cell Death Dis (Li M, Han Y, Xu H*. 2018 Jan 24;9(2):91, IF 5.959)等雜志上。

Abstract

Several important micropeptides encoded by noncoding RNAs have been identified in recent years; however, there have never been any reports of micropeptides in head and neck squamous cell carcinoma (HNSCC). Here we report the discovery and characterization of a human endogenous peptide named micropeptide inhibiting actin cytoskeleton (MIAC). Comprehensive analysis of the TCGA (The Cancer Genome Atlas) database (n = 500), clinical fresh samples (n = 94), and tissue microarrays (n = 60) revealed that lower MIAC expression is correlated with poor overall survival of HNSCC patients. Meanwhile, RNA-sequencing analysis of 9657 human tissues across 32 cancer types from TCGA cohorts found that MIAC is significantly associated with the progression of 5 other different tumors. Mechanistically, MIAC directly interacts with AQP2 (Aquaporin 2) to inhibit the actin cytoskeleton by regulating SEPT2 (Septin 2)/ITGB4 (Integrin Beta 4) and ultimately suppressing the tumor growth and metastasis of HNSCC. Collectively, the mechanism investigation and evaluation of MIAC activity in vivo and in vitro highlights that MIAC plays an important role in HNSCC tumorigenesis.