MicroRNA-26b-5p suppresses the proliferation of tongue squamous cell carcinoma via targeting proline rich 11 (PRR11)

Bioengineered

Hailin Zhang¹  Sha Li¹  Jie Dai¹  Zan Li¹  Anji Xu¹  Chenhui Luo²  Yazhou Xiao²  Ying Liu³  Huayi Ren⁴  Xiao Zhou⁵  Liang Yi⁵  Mingjing Peng⁶  Ying Long⁶ 

[1] Department of Head & Neck Surger;Hunan Provincial Clinical Research Centre for Oncoplastic Surgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P. R. Chin;Hunan Provincial Clinical Research Centre for Oncoplastic Surgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P. R. Chin;Hunan Traditional Chinese Medical College, Zhuzhou, Hunan, P. R. Chin;Translational Medicine Centr;Translational Medicine Centr;Department of Head & Neck Surger;Hunan Provincial Clinical Research Centre for Oncoplastic Surgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P. R. Chin;Translational Medicine Centr;Hunan Provincial Clinical Research Centre for Oncoplastic Surgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P. R. Chin;

关键词: Mir-26b-5p;    prr11;    cell cycle;    tongue squamous cell carcinoma;    proliferation;   

DOI  :  10.1080/21655979.2021.1969832

来源: Taylor & Francis

【 摘 要 】

MicroRNAs (miRNAs) have been proved to be involved in many biological processes during tumorigenesis and progression, including cell proliferation and cell cycle progression. However, the potential role of miR-26b-5p in tongue squamous cell carcinoma (TSCC) remains unclear. In the present study, we demonstrated that miR-26b-5p was decreased in TSCC tissues in both TCGA-TSCC subset and eight paired samples from TSCC patients, while Proline Rich 11 (PRR11) was obviously increased. Transfection of miR-26b-5p mimics inhibited CALL7 cell proliferation by arresting the cells at the S/G2 transition. Meanwhile, miR-26b-5p inhibitor had the opposite biological functions. The results of luciferase activity and RNA-pulldown assays indicated that miR-26b-5p directly targeted the PRR11 3ʹ -untranslated region in CAL27 cells. Furthermore, the effects of miR-26b-5p on cell cycle regulation were reversed after treatment with siRNA against PRR11. In summary, our findings indicate that miR-26b-5p induce cell cycle arrest in TSCC by targeting PRR11. Hence, targeting miR-26b-5p could be a promising therapeutic strategy for the treatment of TSCC.

【 授权许可】

CC BY