LINC01011 promotes colon cancer progression by regulating ferroptosis via the miR-495-3p/SCD axis

Colon cancer (CC) continues to be a major cause of cancer-related deaths globally. LncRNAs have emerged as critical regulators of tumor progression, including ferroptosis. This study evaluated the role of LINC01011 in CC. LINC01011 expression was analyzed using TCGA data and qRT-PCR in CC cell lines. Kaplan-Meier curve was analyzed to evaluate prognostic value. Functional overexpression and silencing experiments were performed in HCT116 and SW480 cells. Cell viability, migration, and colony formation were assessed, along with ferroptosis-related indicators, including Fe²⁺, MDA, 4-HNE, GPX4, and ACSL4. Dual-luciferase reporter assays were conducted to validate interactions among LINC01011, miR-495-3p, and Stearoyl-CoA Desaturase (SCD). Rescue experiments were executed to corroborate the proposed regulatory axis. LINC01011 was significantly upregulated in CC and linked to unfavorable prognosis in TCGA datasets. LINC01011 was increased in HCT116, LoVo, SW480, HT-29 cell lines. Elevated LINC01011 promoted tumor cell viability, migration, and colony formation while suppressing ferroptosis. LINC01011 directly targeted miR-495-3p and negatively regulated its expression. miR-495-3p was downregulated in CC cell lines and targeted SCD, which was upregulated. miR-495-3p overexpression or SCD silencing attenuated the tumor-promoting and anti-ferroptotic effects of LINC01011. Conversely, miR-495-3p inhibition or SCD overexpression abrogated the effects of LINC01011 knockdown. LINC01011 promotes the oncogenic progression of CC cells by modulating ferroptosis via the miR-495-3p/SCD axis.