Chen Xiaofan, Mao Guangxian, Chen Hua, Liu Suyue, Wang Sichao, Li Xiaoqiang, Ye Yiwang, Wu Hao, Liu Jixian
Biomedical Research Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, China.
Department of Thoracic Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Cell Mol Biol (Noisy-le-grand). 2018 Mar 31;64(4):6-10.
B cell leukemia-2 (Bcl-2) plays important roles in the development of tumor and drug resistance. The growth of tumor cells can be inhibited by downregulating the abnormal expression of Bcl-2 protein. TW37, an effective inhibitor of Bcl-2 protein, has now been widely studied in many tumors. In our study, it was found that TW37 exerted a significant effect on the proliferation, apoptosis and migration of Non-Small Cell Lung Cancer cells. Bcl-2 is also a key downstream factor of many signaling pathways such as Epidermal Growth Factor Receptor (EGFR). TW37 enhanced the inhibition of tumorigenesis by gefitinib, an EGFR-Tyrosine Kinase Inhibitor drug. Moreover, TW37 can promote apoptosis ability by inhibiting the phosphorylation level of EGFR protein in H1975 cells. Overall, TW37 enhances the pro-apoptosis and anti-migration ability of gefitinib in Non-Small Cell Lung Cancer.
B细胞淋巴瘤-2（Bcl-2）在肿瘤发生及耐药过程中发挥重要作用。下调Bcl-2蛋白的异常表达可抑制肿瘤细胞生长。TW37作为一种有效的Bcl-2蛋白抑制剂，目前已在多种肿瘤中得到广泛研究。在我们的研究中，发现TW37对非小细胞肺癌细胞的增殖、凋亡及迁移具有显著影响。Bcl-2也是许多信号通路（如表皮生长因子受体（EGFR））的关键下游因子。TW37增强了表皮生长因子受体-酪氨酸激酶抑制剂药物吉非替尼对肿瘤发生的抑制作用。此外，TW37可通过抑制H1975细胞中EGFR蛋白的磷酸化水平来提高凋亡能力。总体而言，TW37增强了吉非替尼在非小细胞肺癌中的促凋亡及抗迁移能力。
Zotero 插件