1. Academic Validation
  2. Myricetin inhibits 4 T1 breast tumor growth in mice via induction of Nrf-2/GPX4 pathway-mediated Ferroptosis

Myricetin inhibits 4 T1 breast tumor growth in mice via induction of Nrf-2/GPX4 pathway-mediated Ferroptosis

  • Toxicol Appl Pharmacol. 2024 Jul:488:116990. doi: 10.1016/j.taap.2024.116990.
Xiaomin Niu 1 Xuhao Ding 2 Qing Tong 3 Xueru Huang 2 Xiaolan Ma 2 Ziping Li 2 Qian Wang 4 Yi Wang 5
Affiliations

Affiliations

  • 1 First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, China; Post Graduate School of Jinzhou Medical University, Jinzhou, Liaoning 121000, China; Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, China.
  • 2 Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, China.
  • 3 Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, China. Electronic address: tongq@jzmu.edu.cn.
  • 4 First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, China.
  • 5 First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, China; Key Surgical Laboratory of Educational Administration of Liaoning Province, Jinzhou Medical University, Jinzhou, Liaoning 121000, China. Electronic address: wangy5@jzmu.edu.cn.
Abstract

Ferroptosis is a recently identified form of programmed cell death that is iron-dependent and closely involved in the pathogenesis of breast Cancer. Past studies have identified myricetin as being able to inhibit breast Cancer growth through its targeting of apoptotic mechanisms, but the precise mechanisms whereby it exerts its antitumoral effects in breast Cancer remain to be characterized in detail. Here, the effects of myricetin on the induction of Ferroptosis in breast Cancer cells were investigated. It was found that myricetin was able to significantly inhibit 4 T1 tumor cell viability and colony forming activity, increasing the level of MDA, Fe2+, and ROS within these cells. From a mechanistic perspective, myricetin was found to induce ferroptotic 4 T1 cell death via downregulating Nrf-2 and GPX4. In vivo experimentation demonstrated that myricetin treatment was sufficient to reduce the growth of subcutaneous breast tumors in female mice as evidenced by decreases in tumor weight and volume, while significantly inhibiting Nrf-2 and GPX4 expression within the tumors of treated mice. Myricetin is capable of readily suppressing breast tumor growth in mice via the induction of ferroptotic activity through the Nrf-2/GPX4 pathway. Myricetin may thus offer utility as a therapeutic agent for the management of breast Cancer in clinical settings.

Keywords

Breast cancer; Ferroptosis; GPX4; Myricetin; Nrf-2.

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