Figure 3.

An illustration showing signaling pathways involved in regulating ferroptosis in lung cancer and their possible crosstalk together. MAPK activation leads to GPX4 inhibition and NOX4 activation (↑ Ferroptosis). SCD1 stabilization by EGFR via its Y55 phosphorylation inhibits ferroptosis through aberrant lipid metabolism (↓ Ferroptosis). Under the hypoxic condition, EGLNs degrades HIF-1α. Therefore, LSH expression is increased and induces SCD1 expression (↓ Ferroptosis). LSH can upregulate lncRNA-LINC00336. This interaction results in CBS inhibition via sponging/inhibiting MIR6852 (↓ Ferroptosis). In addition, LSH downregulates lncRNA-NEAT1 and inhibits p53 via G3BP1 downregulation (↓ Ferroptosis). Upregulation of SAT1 by p53 promotes ferroptosis, and RNF113A deficiency causes ferroptosis by increasing SAT1. Two drugs induce the expression of p53 and drive the cell toward ferroptosis (↑ Ferroptosis). ΔNp63α inhibits ferroptosis. USP35 overexpression leads to ferroptosis suppression by stabilization of FPN (↑ Ferroptosis). Moreover, FPN is inhibited upon decreased expression of miR-302a-3p (↑ Ferroptosis). Zinc intoxication causes ferroptosis by inhibition of the System ${\mathrm{X}}_{\mathrm{c}}^{-}$ inhibition circumstances, glutamate is accumulated in the cell, which results in the calcium ions accumulation. This accumulation induces ferroptosis by CaM and ADCY10 activation (↑ Ferroptosis). Erianin activates CaM (↑ Ferroptosis). USP14 inhibition by 6-Gingerol leads to autophagy induced ferroptosis (↑ Ferroptosis).