Fig. 3

Linc01056 knockdown induced metabolic shift towards fatty acid oxidation. (a). Proteomic analysis on sorafenib-treated MHCC97L cells with or without Linc01056 knockdown. Pathway enrichment on differential gene expression showed that (b) increased genes enriched in pathways related to fatty acid oxidation, while c) reduced genes enriched in pathways related to glycolysis/gluconeogenesis. (d) Changes in expression of FAO-related proteins upon Linc01056 knockdown. (e) GSEA analysis showed enrichment of genes related to FAO. (f) Linc01056 knockdown maintained cellular ATP level upon sorafenib treatment in HCC cells. Knockdown of Linc01056 (g) increased the OCR and (h) decreased the ECAR in HCC cells in the presence of sorafenib. Linc01056 knockdown (i) increased mitochondrial ROS, and (j) maintained the basal respiratory and (k) maximal respiratory capacity in sorafenib-treated HCC cells. (l) Linc01056 increased fatty acid storage in sorafenib-treated HCC cells.(m) Linc01056 knockdown increased content of C16 intermediates of fatty acid in sorafenib-treated HCC cells. *p < 0.05, **p < 0.01, ***p < 0.001