2. Academic Validation
  3. Coptisine-mediated downregulation of E2F7 induces G2/M phase arrest in hepatocellular carcinoma cells through inhibition of E2F4/NFYA/NFYB transcription factors

Coptisine-mediated downregulation of E2F7 induces G2/M phase arrest in hepatocellular carcinoma cells through inhibition of E2F4/NFYA/NFYB transcription factors

  • Chem Biol Interact. 2024 May 23:397:111063. doi: 10.1016/j.cbi.2024.111063.
Hongmei Wang 1,  Zhengcai Ma 2,  Minmin Xu 3,  Mengyuan Xiong 4,  Xiantao Chen 5,  Yuan Zhou 6,  Wanyu Tang 7,  Xuegang Li 8,  Wanqun Chen 9,  Hang Ma 10,  Xiaoli Ye 11
Affiliations

Affiliations

  • 1 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 1289306646@qq.com.
  • 2 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 276940978@qq.com.
  • 3 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 719179358@qq.com.
  • 4 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 1838026532@qq.com.
  • 5 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 1042084283@qq.com.
  • 6 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 543991259@qq.com.
  • 7 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: 2558807060@qq.com.
  • 8 School of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China. Electronic address: Xuegangli@swu.edu.cn.
  • 9 Department of Gastroenterology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, 400000, China. Electronic address: cwq20130219@163.com.
  • 10 School of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China. Electronic address: hangma@swu.edu.cn.
  • 11 Engineering Research Center of Coptis Development & Utilization (Ministry of Education), School of Life Sciences, Southwest University, Chongqing, 400715, China. Electronic address: yexiaoli@swu.edu.cn.
PMID: 38795876 DOI: 10.1016/j.cbi.2024.111063
Abstract

Coptisine (COP) has been shown to exhibit a wide range of Anticancer properties, including in hepatocellular carcinoma (HCC). Nevertheless, the precise mechanism of COP in the treatment of HCC remains elusive. This study aims to investigate the potential mechanism of action of COP against HCC. By evaluating the anti-HCC activity of COP in different HCC cells lines and in xenografted nude mice, it was found that COP inhibited HCC in vitro and in vivo. Through RNA-Seq analysis, E2F7 was identified as a potential target of COP against HCC, as well as the cell cycle as a possible pathway. The overexpression of E2F7 and the inhibition of Chk1 demonstrated that COP inhibits the activity of HCC and induces G2/M phase arrest of HCC cells by down-regulating E2F7 and influencing the Chk1/CDC25A pathway. Finally, the promoter fragmentation experiments and chromatin immunoprecipitation revealed that COP down-regulated E2F7 by inhibiting the E2F4/NFYA/NFYB transcription factors. In conclusion, our study demonstrated that COP downregulates E2F7 by affecting key transcription factors, thereby inducing cell cycle arrest and inhibits HCC cell growth. This provides further evidence of the efficacy of COP in the treatment of tumors.

Keywords

Cell cycle; Coptisine; E2F7; Hepatocellular carcinoma; Transcription factors.

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