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Comment
. 2023 Sep 8;8(1):336.
doi: 10.1038/s41392-023-01593-3.

Cancer cells evade ferroptosis: sex hormone-driven membrane-bound O-acyltransferase domain-containing 1 and 2 (MBOAT1/2) expression

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Comment

Cancer cells evade ferroptosis: sex hormone-driven membrane-bound O-acyltransferase domain-containing 1 and 2 (MBOAT1/2) expression

Alexia Belavgeni et al. Signal Transduct Target Ther. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
MBOAT1/2 prevents cell death of cancer cells that are deficient in the two major ferroptosis-surveillance systems GPX4 and FSP1. For cancer cells to proliferate (to sail the open seas) they must prevent ferroptosis (evade the ferroptopus). Ferroptopus is derived from “ferroptosis” and “octopus” which means “Ferroptosis is like an octopus”. Several ferroptosis-surveillance systems biologically emerged. Most cells rely on glutathione peroxidase 4 (GPX4) and the ferroptosis-suppressor protein 1 (FSP1) to survive (in our little cartoon, FSP1 and GPX4 are the masts of the boats). In addition to GPX4 and FSP1, prostate cancer cells produce MBOAT2 downstream of the androgen receptor (AR, the AR shipyard). In contrast, breast cancer cells generate MBOAT1 downstream of the estrogen receptor alpha (ERα, the ER shipyard). MBOAT1 and MBOAT2 can still prevent capsize in the absence of GPX4 and FSP1 (i.e., in stormy weather if the two masts of the ships are destroyed). Only if the keel of MBOAT1 or MBOAT2 breaks, cancer cell death by ferroptosis occurs (death by water influx caused by the ferroptopus)

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References

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