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. 2022 Nov 7;8:449. doi: 10.1038/s41420-022-01234-8

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A The enrichment of m⁶A-modified LINC01468 was detected by the RIP-RT-qPCR assay in the indicated cells. B The negative correlation between the levels of LINC01468 and ALKBH5 was confirmed in 26 pairs of NAFLD-HCC patients. C ALKBH5 expression in HCC was analyzed in HCC tissues and corresponding para-cancerous tissues from 26 pairs of NAFLD-HCC patients. D The online website http://m6avar.renlab.org/ was used to predict the m⁶A modification locus of LINC01468 modified by ALKBH5, followed by confirmation by the luciferase reporter assay. E, F Effect of ALKBH5 overexpression in SNU-449 cells (E) or knockdown in Huh7 cells (F) on LINC01468 expression. G, H Results of RIP-RT-qPCR showing the enrichment of m⁶A-modified LINC01468 following overexpression in SNU-449 cells or silencing in Huh7 cells of ALKBH5. I LINC01468 stability was analyzed in HCC-LM3 cells with ALKBH5 overexpression or silencing in the presence of actinomycin (D). The data represent the means ± S.D (*P < 0.05; **P < 0.01; ****P < 0.001). J A schematic model for a positive feedback loop between LINC01468 and NAFLD-associated hepatocellular carcinoma. NAFLD upregulated the lipogenesis-related lncRNA, LINC01468, which serves as a molecular glue to bind the E3 ligase CUL4A to SHIP2 and induce SHIP2 degradation through ubiquitination. The reduction in SHIP2 protein results in the accumulation of PIP3, recruiting AKT to the plasma membrane, where AKT/mTOR is activated to facilitate lipogenesis and HCC progression.