Abstract
Doxorubicin (DOX) is among the most used anticancer drugs with associated cardiotoxicity. Follistatin-like 3 (FSTL3), a secreted member of the follistatins family that can selectively bind to members of the TGF-β superfamily, is involved in regulation of cardiac hypertrophy and heart failure. FSTL3 is also upregulated in breast and colorectal cancer tumours, is also an unfavourable prognostic indicator for various cancers. We aim to determine the dual role of FSTL3 in prevention of DOX-induced cardiotoxicity and synergistic anti-cancer effects.
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