Targeting ferroptosis to treat colorectal cancer

Hong Yan; Ronan Talty; Caroline H Johnson

doi:10.1016/j.tcb.2022.11.003

Targeting ferroptosis to treat colorectal cancer

Trends Cell Biol. 2023 Mar;33(3):185-188. doi: 10.1016/j.tcb.2022.11.003. Epub 2022 Dec 3.

Authors

Hong Yan¹, Ronan Talty², Caroline H Johnson³

Affiliations

¹ Department of Environmental Health Sciences, Yale School of Public Health, Yale University, New Haven, CT 06510, USA.
² Department of Pathology, Yale School of Medicine, New Haven, CT, USA.
³ Department of Environmental Health Sciences, Yale School of Public Health, Yale University, New Haven, CT 06510, USA. Electronic address: caroline.johnson@yale.edu.

PMID: 36473802
DOI: 10.1016/j.tcb.2022.11.003

Abstract

Ferroptosis has emerged as a promising target for colorectal cancer (CRC) treatment. Although disrupting glutathione metabolism is the primary strategy for ferroptosis induction, additional key pathways link ferroptosis to CRC pathogenesis. Here, we discuss arachidonic acid (AA), energy metabolism, AMP-activated protein kinase (AMPK), phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR), and Hippo signaling, summarize key findings, and propose new conceptual avenues for CRC treatment.

Keywords: colorectal cancer; ferroptosis; metabolism; therapy.

Publication types

Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural

MeSH terms

Colorectal Neoplasms* / drug therapy
Colorectal Neoplasms* / metabolism
Colorectal Neoplasms* / pathology
Ferroptosis*
Humans
Signal Transduction

Abstract

Publication types

MeSH terms

Grants and funding