Chen Qun, Wang Wenjuan, Wang Yali
Department of Endodontics, Hu'nan Xiangya Stomatological Hospital, Central South University Changsha 410000, Hu'nan Province, China.
Department of Dermatology, First People's Hospital of Chenzhou City Chenzhou 423000, Hu'nan Province, China.
Am J Transl Res. 2022 Jul 15;14(7):5215-5227. eCollection 2022.
The purpose of this study was to establish a causal relationship between microRNA (miR-222) and oral squamous cell carcinoma (OSCC).
The cell viability of each treatment group was measured by MTT. The effects of miR-222 on cell metastasis and apoptosis were measured by transwell and flow cytometry. The targeting relationship between miR-222 and CDKN1B was verified by dual-luciferase reporter gene assay and Western blot. Cell derived xenograft was further constructed to verify the effect of miR-222 on tumor growth by observing tumor weight and volume. The proliferation of tumor tissue was determined by hematoxylin-eosin staining and immunohistochemical staining.
Compared with those in adjacent tissues and normal cells, the levels of miR-222 in OSCC tissues and cells were significantly increased (P<0.05). The miR-222 mimic group promoted tumor cell proliferation, migration and cell cycle and inhibited cell apoptosis significantly (P<0.05). The up-regulation of CDKN1B expression inhibited cell viability, migration and invasiveness and promoted the apoptosis of OSCC (P<0.05). The dual-luciferase reporter gene assay found that miR-222 was targeted to CDKN1B and could inhibit fluorescence activity (P<0.05). assays showed that miR-222 could promote tumor growth through CDKN1B (P<0.05).
MiR-222 was significantly upregulated in OSCC tissues and cells and regulated tumor progression by targeting CDKN1B.
本研究旨在建立微小RNA（miR-222）与口腔鳞状细胞癌（OSCC）之间的因果关系。
采用MTT法检测各治疗组的细胞活力。通过Transwell实验和流式细胞术检测miR-222对细胞转移和凋亡的影响。采用双荧光素酶报告基因检测和蛋白质免疫印迹法验证miR-222与CDKN1B的靶向关系。进一步构建细胞源异种移植模型，通过观察肿瘤重量和体积来验证miR-222对肿瘤生长的影响。通过苏木精-伊红染色和免疫组织化学染色检测肿瘤组织的增殖情况。
与相邻组织和正常细胞相比，OSCC组织和细胞中miR-222的水平显著升高（P<0.05）。miR-222模拟物组显著促进肿瘤细胞增殖、迁移和细胞周期进程，并抑制细胞凋亡（P<0.05）。CDKN1B表达上调抑制了OSCC细胞的活力、迁移和侵袭能力，并促进细胞凋亡（P<0.05）。双荧光素酶报告基因检测发现miR-222靶向CDKN1B并可抑制荧光活性（P<0.05）。实验表明miR-222可通过CDKN1B促进肿瘤生长（P<0.05）。
miR-222在OSCC组织和细胞中显著上调，并通过靶向CDKN1B调节肿瘤进展。
