ACSL4 overexpression

In short, ACSL4 regulated OS progression by modulating TGF-β/Smad2 signaling pathway. These findings underscore ACSL4 as a promising therapeutic target for OS patients and contribute novel insights into the pathogenesis of OS.

Finally, we demonstrated that ACSL4 knockdown significantly reduced metastatic lung nodes in vivo. In conclusion, we reveal a novel positive regulatory loop between ZEB2 and ACSL4, which promotes LDs storage to meet the energy needs of breast cancer metastasis, and identify the ZEB2-ACSL4 signaling axis as an attractive therapeutic target for overcoming breast cancer metastasis.

Our findings indicated that ACSL4 inhibited the pathogenesis of NPC, at least through crosstalk between ferroptosis and macrophages, providing potential direction for NPC therapy.

Protein ubiquitination could have a function in influencing the way that ACSL4-induced ferroptosis works mechanically. ACSL4, which is a mediator and monitor of ferroptosis, was lowered in expression in ccRCC and acted as a valuable diagnostic and prognostic biological marker, thus representing a novel promising treatment target for ccRCC.

Our findings indicate that emodin inhibits proliferation and invasion of CRC cells and reduces VEGF secretion and VEGFR1 and VEGFR2 expression by inhibiting ACSL4. This emodin-induced pathway offers insights into the molecular mechanism of its antitumor effect and provides a potential therapeutic strategy for CRC.