Journal
FEBS OPEN BIO
Volume 11, Issue 11, Pages 3101-3114Publisher
WILEY
DOI: 10.1002/2211-5463.13303
Keywords
breast cancer; c-MYC; FTH1; G9a; iron metabolism
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Funding
- University of Sharjah, Sharjah, UAE [1701050126-P, 1901050144]
- Research Institute for Medical and Health Sciences, University of Sharjah UAE
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High expression of ferritin heavy chain (FTH1) in breast cancer is associated with good prognosis, especially in the triple-negative subtype. FTH1 suppresses tumor growth by inhibiting the expression of key oncogenes, such as c-MYC. This suggests a potential therapeutic target for breast cancer treatment.
Overexpression of ferritin heavy chain (FTH1) often associates with good prognosis in breast cancer (BCa), particularly in the triple-negative subtype (triple-negative breast cancer). However, the mechanism by which FTH1 exerts its possible tumor suppressor effects in BCa is not known. Here, we examined the bearing of FTH1 silencing or overexpression on several aspects of BCa cell growth in vitro. FTH1 silencing promoted cell growth and mammosphere formation, increased c-MYC expression, and reduced cell sensitivity to chemotherapy. In contrast, FTH1 overexpression inhibited cell growth, decreased c-MYC expression, and sensitized cancer cells to chemotherapy; silencing of c-MYC recapitulated the effects of FTH1 overexpression. These findings show for the first time that FTH1 suppresses tumor growth by inhibiting the expression of key oncogenes, such as c-MYC.
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