[1] 雷振伟,张瑜,张旭.miR-181a在人类恶性肿瘤中作用机制的研究进展[J].解放军医学院学报,2016,37(11):1204-1207. [2] Song K, Song Y, Zhao XP, et al. Oral cancer/endothelial cell fusion experiences nuclear fusion and acquisition of enhanced survival potential [J]. Exp Cell Res, 2014, 328(1): 156-163. [3] Mohr M, Zaenker KS, Dittmar T. Fusion in cancer: An explanatory model for aneuploidy, metastasis formation, and drug resistance [J]. Methods Mol Biol, 2015, 1313:21-40. [4] 韩生伟,韩伟,胡勤刚. 炎症、低氧与口腔肿瘤的发生发展[J].口腔医学研究,2014,30(10): 1007-1009. [5] Liu X, Liao W, Peng H, et al. miR-181a promotes G1/S transition and cell proliferation in pediatric acute myeloid leukemia by targeting ATM[J]. J Cancer Res Clin Oncol,2016,142(1):77-87. [6] Bisso A, Faleschini M, Zampa F, et al. Oncogenic miR-181a-5p/b affect the DNA damage response in aggressive breast cancer [J]. Cell Cycle,2013,12:1679-1687. [7] 何倩婷,陈丹,刘中华,等.miR-181a对唾液腺腺样囊性癌细胞株侵袭和迁移的影响[J].中华口腔医学研究杂志(电子版),2014,8(6):447-453. [8] Pawelek JM. Tumour-cell fusion as a source of myeloid traits in cancer [J]. Lancet Oncology, 2005, 403(12):988-993. [9] He X, Li B, Shao Y, et al. Cell fusion between gastric epithelial cells and mesenchymal stem cells results in epithelial-to-mesenchymal transition and malignant transformation [J]. BMC cancer, 2015, 15:24. [10] Diepenbruck M, Christofori G. Epithelial-mesenchymal transition (EMT) and metastasis: Yes, no, maybe [J]. Curr Opin Cell Biol, 2016, 43: 7-13. [11] Cirilli I, Giuliani A, Prattichizzo F, et al. P 232. Role of inflamma-mitomiRs miR-146a, miR-181a and miR-34a in regulating mitochondrial dysfunction during replicative senescence of human endothelial cells [J]. Free Radic Biol Med, 2017,108:S98. [12] Song K, Zhu F, Zhang HZ, et al. Tumor necrosis factor-α enhanced fusions between oral squamous cell carcinoma cells and endothelial cells via VCAM-1/VLA-4 pathway [J]. Exp Cell Res, 2012 ,318(14):1707-1715. |