The apoptotic effects of progesterone on breast cancer (MCF-7) and human osteosarcoma (MG-636) cells.

IF 2.2 4区医学 Q3 PHYSIOLOGY

Physiology international Pub Date : 2020-10-09 Print Date: 2020-10-17 DOI:10.1556/2060.2020.00034

H R Motamed, M Shariati, R Ahmadi, S Khatamsaz, M Mokhtari

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引用次数: 6

Abstract

Purpose: Progesterone has been reported to inhibit the proliferation of breast cancer and osteosarcoma cells; however, its inhibitory mechanism has not yet been clarified. The aim of the present study was to clarify the effects of progesterone on apoptosis in breast cancer (MCF-7) and human osteosarcoma (MG-63) cells.

Materials and methods: In this experimental study the cytotoxic effect of progesterone was measured in MCF-7 and MG-63 cells exposed to different concentrations of progesterone using MTT assay, and effective concentrations were identified. The expression levels of the Bax, P53 and Bcl-2 genes were evaluated by real-time PCR, and caspase-3, 8 and 9 activity levels were determined using a colorimetric method. Hoechst staining and flow cytometry were used to confirm apoptosis. The data were statistically analyzed using one-way analysis of variance (ANOVA) and independent-samples t-test.

Results: Compared to the control group, we observed a significant increase in the expression levels of the Bax and P53 genes and the activity levels of caspase-3 and 9, and a significant decrease in the expression level of the Bcl-2 gene in MCF-7 and MG-63 treated with effective concentration of progesterone. The caspase-8 activity level did not change significantly in treated MG-63 but increased in treated MCF-7 cells. Hoechst staining and flow cytometry results confirmed apoptosis in the cells exposed to effective concentration of progesterone.

Conclusions: The cytotoxic effect of progesterone on breast cancer and osteosarcoma cells was mediated by apoptotic pathways. In this context, progesterone triggers the extrinsic and intrinsic apoptotic pathways in MCF-7 cells and induces the intrinsic apoptotic pathway in MG-63 cells.

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黄体酮对乳腺癌(MCF-7)和人骨肉瘤(MG-636)细胞凋亡的影响。

目的:黄体酮有抑制乳腺癌和骨肉瘤细胞增殖的作用;然而，其抑制机制尚未明确。本研究的目的是阐明黄体酮对乳腺癌(MCF-7)和人骨肉瘤(MG-63)细胞凋亡的影响。材料与方法:本实验采用MTT法测定不同浓度孕酮对MCF-7和MG-63细胞的细胞毒作用，并确定其有效浓度。实时荧光定量PCR检测Bax、P53和Bcl-2基因的表达水平，比色法检测caspase-3、8和9的活性水平。赫斯特染色及流式细胞术证实细胞凋亡。采用单因素方差分析(ANOVA)和独立样本t检验对数据进行统计学分析。结果:与对照组相比，我们观察到有效浓度黄体酮处理MCF-7和MG-63中Bax、P53基因表达水平和caspase-3、9活性水平显著升高，Bcl-2基因表达水平显著降低。MG-63处理后的caspase-8活性水平无显著变化，但MCF-7处理后的caspase-8活性水平升高。Hoechst染色和流式细胞术结果证实黄体酮有效浓度下细胞发生凋亡。结论:黄体酮对乳腺癌和骨肉瘤细胞的细胞毒作用是通过凋亡途径介导的。在这种情况下，黄体酮触发MCF-7细胞的外源性和内源性凋亡途径，诱导MG-63细胞的内源性凋亡途径。

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

Physiology international Medicine-Physiology (medical)

CiteScore

3.40

自引率

0.00%

发文量

期刊介绍： The journal provides a forum for important new research papers written by eminent scientists on experimental medical sciences. Papers reporting on both original work and review articles in the fields of basic and clinical physiology, pathophysiology (from the subcellular organization level up to the oranizmic one), as well as related disciplines, including history of physiological sciences, are accepted.