Department of Otolaryngology Head and Neck Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Bioengineered. 2021 Dec;12(1):1766-1772. doi: 10.1080/21655979.2021.1923354.
Investigation of effects of Meis homeobox 2 (MEIS2) on proliferation and apoptosis of thyroid cancer (TC) cells and its specific molecular mechanism is the main purpose of this study. In this study, we found that the expression of MEIS2 was down-regulated in TC tissues and cell lines (B-CPAP, TPC-1 and K1), compared to adjacent histologically normal tissues and normal thyroid cell (Nthy-ori 3-1). Then, overexpression of MEIS2 promoted B-CPAP cell apoptosis and decreased cell proliferation, viability and cell cycle progression. Further studies confirmed that overexpression of MEIS2 could significantly decrease p65 expression in the nucleus of B-CPAP cells. However, the opposite results were presented after interference of MEIS2 expression. Taken together, MEIS2 expression was significantly down-regulated in TC. In addition, MEIS2 could inhibit NF-κB pathway activation, so as to perform both suppression of the viability and proliferation of TC cells and promotion of apoptosis.
本研究旨在探讨同源盒基因 Meis2(MEIS2)对甲状腺癌(TC)细胞增殖和凋亡的影响及其具体的分子机制。研究发现,与相邻组织学正常的组织和正常甲状腺细胞(Nthy-ori 3-1)相比,MEIS2 在 TC 组织和细胞系(B-CPAP、TPC-1 和 K1)中的表达下调。过表达 MEIS2 可促进 B-CPAP 细胞凋亡,降低细胞增殖、活力和细胞周期进程。进一步的研究证实,过表达 MEIS2 可显著降低 B-CPAP 细胞核内 p65 的表达。然而,干扰 MEIS2 表达后则呈现相反的结果。综上所述,MEIS2 在 TC 中表达明显下调。此外,MEIS2 可以抑制 NF-κB 通路的激活,从而抑制 TC 细胞的活力和增殖,促进细胞凋亡。