Fig 2: IGF2BP1 or KDM5B rescued antitumor phenotypes induced by LINC02428 overexpression in Hep3B cells.EdU and CCK-8 assays showed that the upregulation of IGF2BP1 (A, C, D) or KDM5B (B, E, F) impaired the overexpression of the LINC02428-induced suppression of HCC proliferation. Migration and invasion assays indicated that IGF2BP1 (G) or KDM5B (H) overexpression rescued the inhibition of HCC migration and invasion induced by LINC02428 upregulation. I Western blotting showed expression of protein about both upregulation LINC02428 and IGF2BP1. J Western blot assays showed protein levels after LINC02428 and KDM5B upregulation.

Fig 3: KDM5B affects tumor phenotypes via IGF2BP1.A–C EdU assay D CCK-8 assay indicated that KDM5B silencing could suppress HCC proliferation; however, IGF2BP1 upregulation could reverse the inhibition of proliferation. E–G IGF2BP1 overexpression rescued the KDM5B silencing-induced inhibition of migration and invasion in HCC cells. H Western blotting confirmed KDM5B knockdown downregulated IGF2BP1, whereas IGF2BP1 co-transfection reversed KDM5B downregulation.

Fig 4: A schematic diagram.LINC02428 blocked the KDM5B/IGF2BP1 positive feedback loop to inhibit HCC progression.

Fig 5: AUP1 knockdown transcriptionally regulated by KDM5B interferes with the tumor growth in vivo. (A) The images of SiHa tumor-bearing mice and the dissected tumor. (B) The tumor volumes were recorded every two days from the 6th day after injection. (C) The expression of AUP1 and KDM5B was detected using western immunoblot analysis. (D) Ki67 expression in tumor tissues was detected by immunofluorescence staining. (E) Apoptosis was detected using TUNEL staining. ***P<0.001 vs. control group; #P<0.05 and ###P<0.001 vs. sh-AUP1 + oe-NC group. AUP1, ancient ubiquitous protein 1; KDM5B, lysine demethylase 5B; sh-, short hairpin; NC, negative control; oe-overexpressing.