Laboratory Department, Chung-Kang Branch, Cheng-Ching General Hospital, Taichung, Taiwan.
Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Environ Toxicol. 2024 May;39(5):2961-2969. doi: 10.1002/tox.24156. Epub 2024 Feb 2.
Licochalcone A (LicA), a natural compound extracted from licorice root, has been shown to exert a variety of anticancer activities. Whether LicA has such effects on endometrial cancer (EMC) is unclear. This study aims to investigate the antitumor effects of LicA on EMC. Our results show that LicA significantly reduced the viability and induced apoptosis of EMC cells and EMC-7 cells from EMC patients. LicA was also found to induce endoplasmic reticulum (ER) stress, leading to increased expression of ER-related proteins (GRP78/PERK/IRE1α/CHOP) in EMC cell lines. Suppression of GRP78 expression in human EMC cells treated with LicA significantly attenuated the effects of LicA, resulting in reduced ER-stress mediated cell apoptosis and decreased expression of ER- and apoptosis-related proteins. Our findings demonstrate that LicA induces apoptosis in EMC cells through the GRP78-mediated ER-stress pathway, emphasizing the potential of LicA as an anticancer therapy for EMC.
甘草查尔酮 A（LicA）是一种从甘草根中提取的天然化合物，已被证明具有多种抗癌活性。然而，LicA 是否对子宫内膜癌（EMC）有这样的作用尚不清楚。本研究旨在探讨 LicA 对 EMC 的抗肿瘤作用。我们的研究结果表明，LicA 可显著降低 EMC 细胞和源自 EMC 患者的 EMC-7 细胞的活力并诱导其凋亡。LicA 还诱导内质网（ER）应激，导致 EMC 细胞系中 ER 相关蛋白（GRP78/PERK/IRE1α/CHOP）的表达增加。在经 LicA 处理的人 EMC 细胞中抑制 GRP78 的表达可显著减弱 LicA 的作用，导致 ER 应激介导的细胞凋亡减少和 ER 及凋亡相关蛋白的表达降低。这些发现表明，LicA 通过 GRP78 介导的 ER 应激途径诱导 EMC 细胞凋亡，强调了 LicA 作为 EMC 抗癌治疗的潜力。
