Abstract Title:

Chrysin impairs genomic stability by suppressing DNA double-strand break repair in breast cancer cells.

Abstract Source:

Cell Cycle. 2022 Jan 5:1-13. Epub 2022 Jan 5. PMID: 34985375

Abstract Author(s):

Anke Geng, Shiya Xu, Yunxia Yao, Zhen Qian, Xiyue Wang, Jiahui Sun, Jingyuan Zhang, Fangfang Shi, Zhixi Chen, Weina Zhang, Zhiyong Mao, Wen Lu, Ying Jiang

Article Affiliation:

Anke Geng


Chrysin, a natural compound isolated from various plants, such as the blue passion flower (.), exhibits multiple pharmacological activities, such as antitumor, anti-inflammatory and antioxidant activities. Accumulating evidence shows that chrysin inhibits cancer cell growth by inducing apoptosis and regulating cell cycle arrest. However, whether chrysin is involved in regulating genomic stability and its underlying mechanisms in breast cancer cells have not been determined. Here, we demonstrated that chrysin impairs genomic stability in MCF-7 and BT474 cells, inhibits cell survival and enhances the sensitivity of MCF-7 cells to chemotherapeutic drugs. Further experiments revealed that chrysin impairs DNA double-strand break (DSB) repair, resulting in accumulation of DNA damage. Mechanistic studies showed that chrysin inhibits the recruitment of the key NHEJ factor 53BP1 and delays the recruitment of the HR factor RAD51. Thus, we elucidated novel regulatory mechanisms of chrysin in DSB repair and proposed that a combination of chrysin and chemotherapy has curative potential in breast cancers.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Chemotherapeutic : CK(2328) : AC(1086)

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