Ferritin heavy chain (FTH1) exerts significant antigrowth effects in breast cancer cells by inhibiting the expression of c-MYC

被引:28
|
作者
Ali, Amjad [1 ]
Shafarin, Jasmin [1 ]
Abu Jabal, Rola [2 ]
Aljabi, Nour [2 ]
Hamad, Mohamad [1 ,3 ]
Sualeh Muhammad, Jibran [1 ,2 ]
Unnikannan, Hema [1 ]
Hamad, Mawieh [1 ,3 ]
机构
[1] Univ Sharjah, Res Inst Med & Hlth Sci, Sharjah, U Arab Emirates
[2] Univ Sharjah, Dept Basic Med Sci, Coll Med, Sharjah, U Arab Emirates
[3] Univ Sharjah, Dept Med Lab Sci, Coll Hlth Sci, Sharjah 27272, U Arab Emirates
来源
FEBS OPEN BIO | 2021年 / 11卷 / 11期
关键词
breast cancer; c-MYC; FTH1; G9a; iron metabolism; HISTONE METHYLTRANSFERASE G9A; ALPHA-INDUCED APOPTOSIS; H-FERRITIN; IRON-METABOLISM; TRANSFERRIN RECEPTOR; RESISTANCE; MECHANISM; SUBUNIT; MAMMARY; MARKER;
D O I
10.1002/2211-5463.13303
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3101 / 3114
页数:14
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