4.7 Article

Lecanoric acid mediates anti-proliferative effects by an M phase arrest in colon cancer cells

期刊

BIOMEDICINE & PHARMACOTHERAPY
卷 148, 期 -, 页码 -

出版社

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2022.112734

关键词

Lecanoric acid; Atranorin; Evernic acid; M cell cycle arrest; Cyclin B1; CDK1; Lichens

资金

  1. Landesoffensive zur Entwicklung wissenschaftlich-okonomischer Exzellenz (LOEWE) Center Translational Biodiversity Genomics (TBG)
  2. LOEWE Center Novel Drug Targets against Poverty-Related and Neglected Tropical Infectious Diseases (DRUID)

向作者/读者索取更多资源

Lichen extracts containing compounds such as lecanoric acid possess anti-proliferative effects, particularly in cancer cells. Lecanoric acid exerts its anti-proliferative effects by arresting cells in the M phase. Importantly, it does not affect primary immune cells. These findings suggest that lecanoric acid may be a potential candidate for anti-cancer therapy.
Lichen extracts containing, among other compounds, depsides such as evernic acid, atranorin, and lecanoric acid possess anti-proliferative effects. We aimed to identify lichen metabolites that are responsible for the observed anti-proliferative effects. We performed cytotoxicity, cell colony, cell cycle and apoptosis assays in various cell lines or primary immune cells. We analyzed several cell cycle proteins and apoptosis-related proteins to gain insights into the underlying mechanism. All depsides reduced the viability of the tested cell lines (HCT-116, HEK293T, HeLa, NIH3T3, RAW246.7) in a cell line-dependent manner with lecanoric acid being the most effective. Atranorin did not influence the cell cycle or colony formation in HCT-116 cells, but induced apoptosis in HCT-116 cells. Evernic acid showed no anti-proliferative effects. Lecanoric acid inhibited cell colony formation already at 0.03 mu g/ml in HCT-116 cells and induced a G2 cell cycle block in several cell lines. Moreover, lecanoric acid arrested the cell cycle, presumably in the M phase, since expression of cyclin B1 and phosphorylated histone H3 was upregulated, whereas the inactive cyclin-dependent kinase 1 (CDK1) was reduced in HCT116 cells. Most importantly, cell death induced by lecanoric acid was more prominent in cancer cells than in primary human immune and endothelial cells. In conclusion, lecanoric acid seems to mediate its antiproliferative effects via arrest of cells in the M phase. Our data suggest lecanoric acid may be a potential new candidate for anti-cancer therapy, because it has anti-proliferative effects on cancer cell lines, and does not affect primary immune cells.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据