Oxycodone enhances antitumor effect of paclitaxel on human breast cancer SKBR3 cells in vitro.

IF 2.2 4区医学 Q2 MEDICINE, GENERAL & INTERNAL

Clinics Pub Date : 2024-07-30 eCollection Date: 2024-01-01 DOI:10.1016/j.clinsp.2024.100458

Fangfang Liu, Hongmei Yuan, Chenyang Xu, Mingjie Mao, Shanwu Feng

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引用次数: 0

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

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羟考酮可增强紫杉醇对体外人类乳腺癌 SKBR3 细胞的抗肿瘤作用。

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。本研究旨在探讨 OXY 联合 PTX 对人类乳腺癌 SKBR3 细胞增殖、凋亡和迁移的影响及其内在机制：方法：分别采用 CCK-8、集落形成试验、流式细胞仪、Transwell 试验和划痕试验评估 SKBR3 细胞的增殖、凋亡和侵袭。此外，还使用 Western 印迹法检测了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：与对照组相比，OXY（0.25、0.5 和 1 mM）能显著抑制 SKBR3 细胞的活力、集落形成、迁移和侵袭。此外，OXY（0.25、0.5 和 1 mM）还能明显诱导 SKBR3 细胞凋亡，并降低凋亡相关蛋白的水平。此外，与 PTX 组相比，OXY（0.25、0.5 和 1 mM）和 PTX 在体外协同抑制 SKBR3 细胞的增殖。此外，OXY（0.25、0.5 和 1 mM）通过下调 N-cadherin、Becline-1 LC3-Ⅱ、p-Akt 和 p-mTOR 的表达以及上调 E-cadherin 的表达，显著提高了 PTX 诱导的 SKBR3 细胞凋亡。与对照组相比，OXY（1 mM）可诱导 SKBR3 细胞自噬：本研究表明，OXY 可增强 PTX 在体外对乳腺癌的抗肿瘤作用。因此，OXY 与 PTX 的结合可能成为治疗乳腺癌的一种潜在策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinics 医学-医学：内科

CiteScore

4.10

自引率

3.70%

发文量

129

审稿时长

52 days

期刊介绍： CLINICS is an electronic journal that publishes peer-reviewed articles in continuous flow, of interest to clinicians and researchers in the medical sciences. CLINICS complies with the policies of funding agencies which request or require deposition of the published articles that they fund into publicly available databases. CLINICS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration.