Fig. 5

Research has provided a deeper understanding of the significant role played by non-coding RNAs, particularly lncRNAs and circRNAs, in ferroptosis, a form of cell death distinguished by the buildup of lipid peroxidation due to iron. In the context of cancer cells, these particular RNA molecules play a crucial role in controlling ferroptosis processes. This highlights their potential as significant targets for the advancement of groundbreaking treatment methods. An example of this is the lncRNA called LINC00336, which can increase cysteine levels through the CBS pathway, thereby promoting ferroptosis resistance in lung cancer cells. In addition, it downregulates the expression of miRNAs that encourage ferroptosis, such as MIR6852. Based on recent research, another lncRNA called LINC00472 or p53RRA has been discovered to stimulate the activity of the TP53 gene, resulting in heightened levels of ferroptosis in cells affected by lung cancer. These findings demonstrate the immense influence of lncRNAs and circRNAs in the pathways of ferroptosis, implying their potential as valuable targets for the development of novel cancer treatments. PVT1 works together with MIR214 to target TP53 and cause ferroptosis. It does so by reducing the levels of cysteine, which is achieved by suppressing SLC7 A11. Furthermore, LINC00618 involves in sensitizing leukemic cells to ferroptosis. This is achieved by enhancing the levels of ROS and iron accumulation while simultaneously suppressing the expression of SLC7 A11. In the case of ZFAS1, it acts as a competing endogenous RNA (ceRNA) by competing with miR-150 - 5p, thereby reducing the expression of SLC38 A1. This, in turn, regulates glutamine uptake and lipid metabolism, ultimately promoting ferroptosis. LINC01833/RP11–89 also participates in inhibiting ferroptosis in bladder cancer by acting as a ceRNA and soaking up MIR129 - 5p. This leads to the increased expression of PROM2, which facilitates the export of iron through ferritin-containing exosomes. In the case of glioma, CircTTBK2 functions as a circular RNA and governs ferroptosis by acting as a sponge for various miRNAs, most notably MIR761, which targets MFN2. Through its interaction with MIR761, CircTTBK2 boosts the expression of ITGB8, ultimately obstructing the process of ferroptosis in glioma cells. Similarly, Circ_0008367 induces ferroptosis in a manner that relies on autophagy by disrupting ALKBH5's function of promoting autophagy. In contrast, circ_0008035 suppresses ferroptosis in gastric cancer by directly targeting MIR599 and disrupting the regulatory axis of MIR599–EIF4 A1. In addition, CircIL4R and circEPSTI1 can also regulate ferroptosis by influencing the MIR541–3p-GPX4 and MIR375–MIR409–3p-MIR515–5p-SLC7 A11 pathways, respectively. Finally, circSNX12 interacts with MIR224–5p to target FTH1, which regulates iron homeostasis and ferroptosis susceptibility