Progesterone decreases viability and up regulates membrane progesterone receptors expression on the human Chronic Myeloid Leukemia cell line

IF 1.4 4区 医学 Q4 GENETICS & HEREDITY Cancer Genetics Pub Date : 2024-11-01 DOI:10.1016/j.cancergen.2024.10.006
Vahid Bagheri , Fateme Rezaei , Razieh Alipour , Nasrin Sereshki , Vahid Ahmadipanah , Mitra Rafiee
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Abstract

Progesterone (P4) has an important effect (activatory or inhibitory) on cell proliferation. Although there is evidence of the impact of progesterone on sex-linked cancers, it can affect other cancer cells expressing P4 receptors (PRs). We evaluated the expression of membrane P4 receptors (mPRs) and the viability in progesterone-treated K562 cells to inspect the possible effects route of progesterone on this (CML) cancer cell line. K562 cells were exposed to various concentrations of progesterone or no exposure for 48 and 72 h. The percentage of viability and cells that expressed mPRα and mPRβ were evaluated by MTT test and flow cytometry respectively. Progesterone significantly increased the expression of mPRα and especially mPRβ on the surface of K562 cells and significantly decreased their viability (p ≤ 0.05). Progesterone can reduce viability in K562 cells. Our findings showed that progesterone affects its receptor expression on K562 cells. Thus it may influence the performance of K562 cells in addition to its direct effects on these cells (via binding to its receptors).
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孕酮可降低人慢性髓性白血病细胞系的存活率并上调膜孕酮受体的表达。
孕酮(P4)对细胞增殖有重要影响(激活或抑制)。虽然有证据表明黄体酮对性联癌症有影响,但它也会影响其他表达 P4 受体(PRs)的癌细胞。我们评估了经黄体酮处理的 K562 细胞中膜 P4 受体(mPRs)的表达和活力,以研究黄体酮对这种(CML)癌细胞系的可能影响途径。将 K562 细胞暴露于不同浓度的黄体酮或不暴露于黄体酮 48 小时和 72 小时,分别用 MTT 试验和流式细胞术评估其存活率以及表达 mPRα 和 mPRβ 的细胞百分比。结果显示,黄体酮能明显增加 K562 细胞表面 mPRα 的表达,尤其是 mPRβ 的表达,并明显降低其存活率(p ≤ 0.05)。黄体酮可降低 K562 细胞的活力。我们的研究结果表明,黄体酮会影响其在 K562 细胞上的受体表达。因此,除了直接影响 K562 细胞(通过与其受体结合)外,孕酮还可能影响这些细胞的性能。
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来源期刊
Cancer Genetics
Cancer Genetics ONCOLOGY-GENETICS & HEREDITY
CiteScore
3.20
自引率
5.30%
发文量
167
审稿时长
27 days
期刊介绍: The aim of Cancer Genetics is to publish high quality scientific papers on the cellular, genetic and molecular aspects of cancer, including cancer predisposition and clinical diagnostic applications. Specific areas of interest include descriptions of new chromosomal, molecular or epigenetic alterations in benign and malignant diseases; novel laboratory approaches for identification and characterization of chromosomal rearrangements or genomic alterations in cancer cells; correlation of genetic changes with pathology and clinical presentation; and the molecular genetics of cancer predisposition. To reach a basic science and clinical multidisciplinary audience, we welcome original full-length articles, reviews, meeting summaries, brief reports, and letters to the editor.
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