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山豆根碱通过诱导细胞凋亡抑制肺癌细胞生长。

Medicarpin suppresses lung cancer cell growth and by inducing cell apoptosis.

机构信息

College of Life Science and Technology, Innovation Center of Molecular Diagnostics, Beijing University of Chemical Technology, Beijing 100029, China.

Department of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China.

出版信息

Acta Pharm. 2024 Mar 30;74(1):149-164. doi: 10.2478/acph-2024-0006. Print 2024 Mar 1.

DOI:10.2478/acph-2024-0006
PMID:38554387
Abstract

Lung cancer (LC) is the leading cause of cancer deaths worldwide. Surgery, chemoradiotherapy, targeted therapy, and immunotherapy are considered dominant treatment strategies for LC in the clinic. However, drug resistance and meta-stasis are two major challenges in cancer therapies. Medicarpin (MED) is an isoflavone compound isolated from alfalfa, which is usually used in traditional medicine. This study was de sig ned to evaluate the anti-LC effect and reveal the underlying mechanisms of MED and . We found that MED could significantly inhibit proliferation, induce apoptosis, and cell cycle arrest of A549 and H157 cell lines. Basically, MED induced cell apoptosis of LC cells by upregu lating the expression of pro-apoptotic proteins BAX and Bak1, leading to the cleavage of caspase-3 (Casp3). Moreover, MED inhibited the proliferation of LC cells downregulating the expression of proliferative protein Bid. Overall, MED inhibited LC cell growth and suppressing cell proliferation and inducing cell apoptosis, suggesting the therapeutic potential of MED in treating LC.

摘要

肺癌(LC)是全球癌症死亡的主要原因。手术、放化疗、靶向治疗和免疫治疗被认为是 LC 的主要临床治疗策略。然而,耐药性和转移是癌症治疗的两个主要挑战。芒柄花素(MED)是从紫花苜蓿中分离出来的一种异黄酮化合物,通常用于传统医学。本研究旨在评估 MED 的抗 LC 作用,并揭示其潜在机制。我们发现 MED 可显著抑制 A549 和 H157 细胞系的增殖,诱导细胞凋亡和细胞周期停滞。基本上,MED 通过上调促凋亡蛋白 BAX 和 Bak1 的表达诱导 LC 细胞凋亡,导致 caspase-3(Casp3)的裂解。此外,MED 通过下调增殖蛋白 Bid 的表达抑制 LC 细胞的增殖。总体而言,MED 通过抑制细胞增殖和诱导细胞凋亡来抑制 LC 细胞生长,提示 MED 在治疗 LC 方面具有潜在的治疗作用。

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