背景:羟考酮(OXY)联合紫杉醇(PTX)对乳腺癌细胞的影响尚不清楚。本研究旨在研究OXY联合PTX对细胞增殖的影响,凋亡,和人乳腺癌SKBR3细胞的迁移和潜在的机制。
方法:增殖,通过CCK-8,集落形成试验评估SKBR3细胞的凋亡和侵袭,流式细胞术,Transwell分析和划痕分析,分别。此外,使用蛋白质印迹法检测这些细胞中相关蛋白的表达。在透射电子显微镜下观察自噬体。
结果:OXY(0.25、0.5和1mM)显着抑制活力,菌落形成,迁移,与对照组相比,SKBR3细胞的侵袭。此外,OXY(0.25、0.5和1mM)显着诱导SKBR3细胞凋亡和凋亡相关蛋白的水平。此外,与体外PTX组相比,OXY(0.25、0.5和ImM)和PTX协同抑制SKBR3细胞的增殖。此外,OXY(0.25、0.5和1mM)通过下调N-cadherin的表达显着提高PTX诱导的SKBR3细胞凋亡,Becline-1LC3-Ⅱ,p-Akt和p-mTOR和上调E-cadherin表达。与对照组相比,OXY(1mM)处理诱导SKBR3细胞自噬。
结论:本研究表明OXY可以增强PTX对乳腺癌的体外抗肿瘤作用。因此,OXY与PTX的联合应用可能成为治疗乳腺癌的潜在策略.
The influences of
Oxycodone (OXY) combined with Paclitaxel (PTX) on breast cancer cells are unclear. The present study aimed to examine the effects of OXY combined with PTX on the proliferation, apoptosis, and migration of human breast cancer SKBR3 cells and the underlying mechanism.
The proliferation, apoptosis and invasion of SKBR3 cells were assessed by CCK-8, colony formation assay, flowcytometric, Transwell assay and scratch assays, respectively. In addition, Western blotting was used to detect the expression of related proteins in these cells. The autophagic bodies were observed under a transmission electron microscope.
OXY (0.25, 0.5 and 1 mM) significantly inhibited the viability, colony-forming, migration, and invasion of SKBR3 cells as compared to the control group. Furthermore, OXY (0.25, 0.5 and 1 mM) markedly induced the apoptosis of SKBR3 cells and the levels of apoptosis-related proteins. In addition, OXY (0.25, 0.5 and 1 mM) and PTX inhibited the proliferation of SKBR3 cells synergistically as compared to PTX group in vitro. Moreover, OXY (0.25, 0.5 and 1 mM) significantly elevated the PTX-induced apoptosis in SKBR3 cells via downregulating the expression of N-cadherin, Becline-1 LC3-Ⅱ, p-Akt and p-mTOR and upregulating E-cadherin expression. Compared with the control group, OXY (1 mM) treatment induced autophagy in SKBR3 cells.
The present study indicates that OXY can enhance the antitumor effect of PTX on breast cancer in vitro. Hence, the combination of OXY with PTX may serve as a potential strategy for the treatment of breast cancer.