Gao Xiang, Liu Zhenping, Zhong Meifeng, Wu Kunhe, Zhang Yuzhao, Wang Hongmei, Zeng Tao
Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Department of Laboratory Medicine, The People's Hospital of Shajing, Shenzhen, Guangdong 518104, P.R. China.
Oncol Lett. 2019 Jan;17(1):288-293. doi: 10.3892/ol.2018.9597. Epub 2018 Oct 18.
Effective therapy for breast cancer has been extensively studied worldwide, particularly for triple-negative breast cancer and drug-resistant subtypes. DNA/RNA-binding protein KIN17 (kin17) has been reported to be significantly upregulated in breast cancer cells, and is proposed to serve a role in the regulation of cell proliferation. The present study further investigated the association of kin17-knockdown with breast cancer cell apoptosis. Cell Counting kit-8, flow cytometry, TUNEL assay and caspase 3/7 analysis were performed on MDA-MB-231 cells to determine the association between kin17 and breast cancer cell apoptosis. In addition, western blot analysis was performed to investigate the mechanism of kin17 in the apoptosis of MDA-MB-231 cells. The results revealed that knockdown of kin17 inhibited proliferation and promoted apoptosis of MDA-MB-231 cells, and suggested a poly (adenosine diphosphate-ribose) polymerase-related mechanism behind the apoptosis of the cells. These findings suggested that kin17 could become a novel target for breast cancer therapy.
乳腺癌的有效治疗方法已在全球范围内得到广泛研究,尤其是针对三阴性乳腺癌和耐药亚型。据报道,DNA/RNA结合蛋白KIN17(kin17)在乳腺癌细胞中显著上调,并被认为在细胞增殖调控中发挥作用。本研究进一步探讨了敲低kin17与乳腺癌细胞凋亡的关联。对MDA-MB-231细胞进行细胞计数试剂盒-8、流式细胞术、TUNEL检测和半胱天冬酶3/7分析,以确定kin17与乳腺癌细胞凋亡之间的关联。此外,进行蛋白质印迹分析以研究kin17在MDA-MB-231细胞凋亡中的机制。结果显示,敲低kin17可抑制MDA-MB-231细胞的增殖并促进其凋亡,并提示细胞凋亡背后存在聚(二磷酸腺苷-核糖)聚合酶相关机制。这些发现表明,kin17可能成为乳腺癌治疗的新靶点。