Effects of miR-155-3p on the degradation rate of EAF1 mRNA and malignant proliferation in HANK1 cells

doi:10.12047/j.cjap.6159.2021.095

Abstract

Abstract: Objective: To investigate the effects and mechanisms of miR-155-3p on the malignant behavior of human NK/T cell lymphoma cell line HANK1. Methods: Targetscan database was used to predict the target gene of miR-155-3p. HANK1 cells in logarithmic growth period were cultured, and the cells were divided into blank group, over-expressed group, control group and interference group, which were transfected with pENTER-puro vector, pENTER-miR-155-3p vector, GV248 control vector and GV248-miR-155-3p siRNA interference vector, respectively. Meanwhile, actinomycin D (ActD) was used to treat each group of cells, and the expressions of miR-155-3p, EAf1, β-catenin and c-Myc in each group were detected by real-time fluorescence quantitative PCR (n=5). The degradation rate of EAF1 mRNA, the expressions of EAF1, β-catenin and c-Myc protein were detected by Western blot (n=3), and the malignant proliferation abilities of cells were detected by CCK-8 (n=5). Results: Compared with the blank group, the expression levels of miR-155-3p, β-catenin and c-Myc in the over-expressed group were significantly higher, the expression level of EAF1 was lower, the half-life of EAF1 mRNA was shortened, and the malignant proliferation ability of the cells was strengthened (P＜0.05). Compared with the control group, the expression levels of miR-155-3p, β-catenin and c-Myc in the interference group were significantly lower, and the expression level of EAF1 was increased, the half-life of mRNA was prolonged and the ability of cell proliferation was decreased (P＜0.05). Conclusion: miR-155-3p can promote EAF1 mRNA degradation and proliferation in HANK1 cells.

Key words: NK/T cell lymphoma, miR-155-3p, EAF1, cell proliferation

CLC Number:

R363.1

LIU Li, XU Kai, WANG Lu-qiang, XU Mei-li. Effects of miR-155-3p on the degradation rate of EAF1 mRNA and malignant proliferation in HANK1 cells[J]. CJAP, 2021, 37(6): 601-605.

References

[1] 张琪, 江浩, 周咏春. 结外鼻型NK/T细胞淋巴瘤放化疗研究进展[J]. 现代肿瘤医学, 2018(1): 132-136.
[2] Tang B, Lei B, Qi G, et al. MicroRNA-155-3p promotes hepatocellular carcinoma formation by suppressing FBXW7 expression[J]. J Exp Clin Cancer Res, 2016, 35(1): 93.
[3] Zhang G, Zhong L, Luo H, et al. MicroRNA-155-3p promotes breast cancer progression through down-regulating CADM1[J]. Onco Targets Ther, 2019, 12(2): 7993-8002.
[4] Polak PE, Simone F, Kaberlein JJ, et al. ELL and EAF1 are Cajal body components that are disrupted in MLL-ELL leukemia[J]. Mol Biol Cell, 2003, 14(4): 1517-1528.
[5] Liu JX, Zhang D, Xie X, et al. Eaf1 and Eaf2 negatively regulate canonical Wnt/β-catenin signaling[J]. Development, 2013, 140(5): 1067-1078.
[6] 梁宛伶, 肖天保, 袁峰, 等. miRNA-95靶向FOXD1基因对结直肠癌LoVo细胞放射敏感性的影响及其机制[J]. 中国应用生理学杂志, 2020, 36(2): 148-151.
[7] Chen G, Chen Z, Zhao H. MicroRNA-155-3p promotes glioma progression and temozolomide resistance by targeting Six1[J]. J Cell Mol Med, 2020, 24(9):5363-5374.
[8] Tao M, Zhou Y, Jin Y, et al. Blocking lncRNA MIR 155HG/miR-155-5p/-3p inhibits proliferation, invasion and migration of clear cell renal cell carcinoma[J]. Pathol Res Pract, 2020, 216(2):152803.
[9] Fonte E, Apollonio B, Scarfò L, et al. In vitro sensitivity of CLL cells to fludarabine may be modulated by the stimulation of Toll-like receptors[J]. Clin Cancer Res, 2013, 19(2): 367-379.
[10] Li Y, Takahashi Y, Fujii S, et al. EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity[J]. Nat Commun, 2016, 7: 10836.
[11] Simone F, Luo RT, Polak PE, et al. ELL-associated factor 2 (EAF2), a functional homolog of EAF1 with alternative ELL binding properties[J]. Blood, 2003, 101(6): 2355-2362.
[12] Polak PE, Simone F, Kaberlein JJ, et al. ELL and EAF1 are Cajal body components that are disrupted in MLL-ELL leukemia[J]. Mol Biol Cell, 2003, 14(4): 1517-1528.
[13] Shilatifard A, Haque D, Conaway RC, et al. Structure and function of RNA polymerase II elongation factor ELL. Identification of two overlapping ELL functional domains that govern its interaction with polymerase and the ternary elongation complex[J]. J Biol Chem, 1997, 272(35): 22355-22363.
[14] Luo RT, Lavau C, Du C, et al. The elongation domain of ELL is dispensable but its ELL-associated factor 1 interaction domain is essential for MLL-ELL-induced leukemogenesis[J]. Mol Cell Biol, 2001, 21(16): 5678-5687.
[15] VanAndel H, Kocemba KA, Spaargaren M, et al. Aberrant Wnt signaling in multiple myeloma: molecular mechanisms and targeting options[J]. Leukemia, 2019, 33(5): 1063-1075.
[16] Wang B, Tian T, Kalland KH, et al. Targeting Wnt/β-catenin signaling for cancer immunotherapy[J]. Trends Pharmacol Sci, 2018, 39(7): 648-658.
[17] Pascal LE, Su F, Wang D, et al. Conditional deletion of Eaf1 induces murine prostatic intraepithelial neoplasia in mice[J]. Neoplasia, 2019, 21(8): 752-764.