Abstract
Ferroptosis is an emerging programmed cell death and plays essential roles in tumorigenesis, including colorectal cancer (CRC). The present study intended to disclose the role of a novel oncogene circular RNA (circRNA) circSTIL in CRC phenotypes, especially ferroptosis. The expression of circSTIL was measured in CRC tissues and cells. Then, the impacts of circSTIL expression on the proliferation and ferroptosis of CRC cells were examined by loss-of-function assays in vitro. Bioinformatics, luciferase reporter assay and cell rescue assay were further performed to reveal the ceRNA-associated mechanism of circSTIL. CircSTIL was significantly upregulated in CRC. Cell proliferation was suppressed while ferroptosis was induced with the silencing of circSTIL in CRC cells. Interestingly, circSTIL competed with miR-431 for solute carrier family 7 member 11 (SLC7A11) binding. Additionally, miR-431 suppression or SLC7A11 overexpression overturned circSTIL silencing-mediated cell phenotypes in CRC cells. CircSTIL promotes CRC cell proliferation and suppresses ferroptosis in vitro via miR-431/SLC7A11 signaling, revealing the pathogenesis of CRC, and providing potential therapeutic targets of CRC.