mTORC1 and ferroptosis: Regulatory mechanisms and therapeutic potential

Bioessays 43 (8):2100093 (2021)
  Copy   BIBTEX

Abstract

Ferroptosis, a form of regulated cell death triggered by lipid hydroperoxide accumulation, has an important role in a variety of diseases and pathological conditions, such as cancer. Targeting ferroptosis is emerging as a promising means of therapeutic intervention in cancer treatment. Polyunsaturated fatty acids, reactive oxygen species, and labile iron constitute the major underlying triggers for ferroptosis. Other regulators of ferroptosis have also been discovered recently, among them the mechanistic target of rapamycin complex 1 (mTORC1), a central controller of cell growth and metabolism. Inhibitors of mTORC1 have been used in treating diverse diseases, including cancer. In this review, we discuss recent findings linking mTORC1 to ferroptosis, dissect mechanisms underlying the establishment of mTORC1 as a key ferroptosis modulator, and highlight the potential of co‐targeting mTORC1 and ferroptosis in cancer treatment. This review will provide valuable insights for future investigations of ferroptosis and mTORC1 in fundamental biology and cancer therapy.

Links

PhilArchive



    Upload a copy of this work     Papers currently archived: 91,709

External links

Setup an account with your affiliations in order to access resources via your University's proxy server

Through your library

Similar books and articles

Regulatory options for gender equity in health research.Belinda Bennett & Isabel Karpin - 2008 - International Journal of Feminist Approaches to Bioethics 1 (2):80-99.
Time to Stop Worrying about the Therapeutic Misconception.David S. Wendler - 2012 - Journal of Clinical Ethics 23 (3):272-287.
Persistent Professional Outcry Needed.Iliya Valkov - 2019 - Journal of Media Ethics 38 (2):iii-v.

Analytics

Added to PP
2022-11-21

Downloads
9 (#1,249,590)

6 months
7 (#421,763)

Historical graph of downloads
How can I increase my downloads?

Citations of this work

No citations found.

Add more citations

References found in this work

No references found.

Add more references