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Ferritinophagy is not required for colon cancer cell growth
Author(s) -
Hasan Mazen,
Reddy Sreedhar M.,
Das Nupur K.
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11439
Subject(s) - autophagy , biology , colorectal cancer , cancer research , cell growth , knockout mouse , cancer cell , transferrin , cancer , microbiology and biotechnology , intracellular , receptor , endocrinology , apoptosis , biochemistry , genetics
Ferritinophagy is a form of selective autophagy responsible for degrading intracellular ferritin, mediated by nuclear receptor coactivator 4 (NCOA4). NCOA4 plays significant roles in systemic iron homeostasis, and its disruption leads to simultaneous anemia and susceptibility to iron overload. The importance of iron colorectal cancer pathogenesis is well studied; however, the role of ferritinophagy in colon cancer cell growth has not been assessed. Disruption of ferritinophagy via NCOA4 knockout leads to only marginal differences in growth under basal and iron‐restricted conditions. Moreover, NCOA4 played no significant role in cell death induced by 5‐fluorouracil and erastin. Western blotting analysis for ferritin and transferrin receptor 1 found a dose‐dependent effect on expression in both proteins in wild‐type and NCOA4 knockout cell lines, but further investigation revealed no difference in growth response when treated at both high and low doses. Our data demonstrate a marginal role for ferritinophagy in growth both under normal and cytotoxic conditions in colon cancer cells, as well as a possible compensatory mechanism in colon cancer cells in response to ferroptosis induction.