LINC01929 promotes breast cancer progression through a TFRC-associated ferroptosis pathway.
TL;DR
It is suggested that targeting LINC01929 to regulate TFRC-mediated ferroptosis could represent a promising therapeutic strategy for BC, positioning both LINC01929 and TFRC as potential biomarkers and therapeutic targets.
Abstract
Breast cancer (BC) remains the most prevalent malignancy among women worldwide, with persistent challenges such as drug resistance and tumor progression despite significant therapeutic advancements. The roles of ferroptosis and long non-coding RNAs (lncRNAs) in BC are not yet fully elucidated, underscoring the need for novel therapeutic targets. In this study, we investigated the function of LINC01929 in BC through a combination of in vitro and in vivo experiments, bioinformatics analysis, RNA pull-down mass spectrometry, and clinical tissue validation. We found that LINC01929 is significantly overexpressed in BC tissues and is associated with poor patient prognosis. Mechanistically, LINC01929 promoted malignant phenotypes in BC cells and was associated with reduced ferroptosis-related stress, with these effects being at least partly dependent on transferrin receptor (TFRC). Conversely, silencing LINC01929 led to reduced TFRC expression and induced ferroptosis in BC cells. Clinical data further confirmed that elevated TFRC levels correlate with aggressive tumor features and unfavorable outcomes. These findings suggest that targeting LINC01929 to regulate TFRC-mediated ferroptosis could represent a promising therapeutic strategy for BC, positioning both LINC01929 and TFRC as potential biomarkers and therapeutic targets.