Fig 2: Impact of the lipokine PI(18:1/18:1) on stress (-adaptive) signaling.SCD1-derived PI(18:1/18:1) (i) interferes with the UPR and autophagy, (ii) prevents the activation of p38 MAPK via MKK3/6, (iii) maintains cell morphology and supports cell proliferation, (vi) diminishes the induction of programmed cell death, and (vii) its content is regulated in various stress-related processes such as tumorigenesis, chemoresistance, aging, starvation, and infection.

Fig 3: Upregulation of lipogenic enzyme SCD1 in CPT2-depleted HepG2 cells. (A) qRT-PCR analysis for mRNA expression of lipogenic enzyme genes ACLY, ACC1, FASN, and SCD1 in HepG2 cells as indicated. Data are presented as the mean ± SD from three independent experiments. (B) Western blot analysis for protein levels of SCD1 in the indicated cells. (C) Schematic model depicting the activation of lipogenesis by CPT2 downregulation which in turn promotes proliferation, metastasis, and chemoresistance in HCC. *P<0.05; **P<0.01.Abbreviations: CPT2, carnitine palmitoyltransferase-2; HCC, hepatocellular carcinoma; qRT-PCR, quantitative reverse transcriptase polymerase chain reaction.

Fig 4: In vivo role of the USP7/hnRNPA1/lncFERO pathway in regulating ferroptosis and chemosensitivity of gastric tumors.A Schematic description of the experimental design used to establish the animal model. B Images and the diameters of tumors in each group (n = 6). C Weight measurements of the tumors described above (n = 6). D WB analysis of USP7, hnRNPA1 and SCD1 in tumor tissues (n = 3). E Quantitative analysis of (D) (n = 3). F Relative levels of serum exo-lncFERO in each group (n = 6). G Relative levels of SCD1 mRNA in tumor tissues (n = 6). H Relative levels of PUFAs in tumor tissues (n = 6). I, J Quantification of a ferroptosis marker (I) and an apoptosis marker (J) in each group (n = 6). K, L Kaplan–Meier curves of mice in the saline-treated groups (K) and cisplatin-treated groups (L) (n = 6). **p < 0.01.

Fig 5: Exosomal lncFERO is positively linked with SCD1 expression.A Serum exosomes were observed by using an electron microscope (scale bar, 200 nm). B Detection of exosome markers, Tsg101, CD9, and Alix, by western blotting assay. C Nanotracking analysis of the diameters of vesicles. E Relative levels of exo-lncFERO in normal subjects (n = 104) and GC patients (n = 112). F Relative levels of exo-lncFERO in the exos and exo-free serum (n = 10). G Exo-lncFERO is positively correlated with SCD1 (n = 112). H Exo-lncFERO is negatively correlated with lipid ROS levels (n = 112). **p < 0.01.