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吉马酮通过调节HBXIP介导的细胞周期、凋亡并促进自噬体形成来抑制胃癌细胞增殖。

Germacrone Regulates HBXIP-Mediated Cell Cycle, Apoptosis and Promotes the Formation of Autophagosomes to Inhibit the Proliferation of Gastric Cancer Cells.

作者信息

Fang Xing, Tan TingFei, Gao BeiBei, Zhao YingLi, Liu TingTing, Xia Quan

机构信息

Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Department of Pharmacy, The Second People's Hospital of Hefei, Hefei, China.

出版信息

Front Oncol. 2020 Nov 10;10:537322. doi: 10.3389/fonc.2020.537322. eCollection 2020.

DOI:10.3389/fonc.2020.537322
PMID:33244453
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7683780/
Abstract

Germacrone, a monocyclic sesquiterpene, exerts marked antitumor effects in a variety of cancers, including hepatocellular carcinoma, gastric cancer, and breast cancer. However, the mechanism underlying the effects of germacrone on gastric cancer remains unclear. In this study, we show that germacrone inhibited gastric cancer cell proliferation in a dose-dependent manner, and induced G0/G1-phase cell cycle arrest and apoptosis in these cells. Moreover, germacrone increased the expression of LC3II/LC3I. And LC3II/LC3I was significant increased after germacrone treatment compared with germacrone and bafilomycin A1 (Baf A1) treatment, which suggested germacrone promoted the formation of autophagosomes. Proteomic analysis was then used to identify molecular targets of germacrone in gastric cancer. A total of 596 proteins were screened, and the top hit was identified as late endosomal/lysosomal adaptor and MAPK and MTOR activator 5 (LAMTOR5, also named HBXIP). Overexpression of HBXIP delayed the germacrone-induced cell cycle arrest, induction of apoptosis, and inhibition of autophagy. Combined, our results indicate that germacrone suppresses gastric cancer cell proliferation by inhibiting HBXIP, and this process is related to G0/G1-phase arrest and apoptosis.

摘要

吉马酮是一种单环倍半萜，对多种癌症具有显著的抗肿瘤作用，包括肝细胞癌、胃癌和乳腺癌。然而，吉马酮对胃癌作用的潜在机制仍不清楚。在本研究中，我们发现吉马酮以剂量依赖性方式抑制胃癌细胞增殖，并诱导这些细胞发生G0/G1期细胞周期阻滞和凋亡。此外，吉马酮增加了LC3II/LC3I的表达。与吉马酮和巴弗洛霉素A1（Baf A1）处理相比，吉马酮处理后LC3II/LC3I显著增加，这表明吉马酮促进了自噬体的形成。随后进行蛋白质组学分析以鉴定吉马酮在胃癌中的分子靶点。共筛选出596种蛋白质，其中排名第一的被鉴定为晚期内体/溶酶体衔接蛋白以及MAPK和MTOR激活剂5（LAMTOR5，也称为HBXIP）。HBXIP的过表达延迟了吉马酮诱导的细胞周期阻滞、凋亡诱导和自噬抑制。综合来看，我们的结果表明吉马酮通过抑制HBXIP来抑制胃癌细胞增殖，并且这个过程与G0/G1期阻滞和凋亡有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a76/7683780/6d17627eae5c/fonc-10-537322-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a76/7683780/f15710027fe9/fonc-10-537322-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a76/7683780/6d17627eae5c/fonc-10-537322-g007.jpg

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