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Fig. 8 | Molecular Cancer

Fig. 8

From: ALKBH5 suppresses malignancy of hepatocellular carcinoma via m6A-guided epigenetic inhibition of LYPD1

Fig. 8

Low ALKBH5 expression is interrelated with high LYPD1 expression in HCC. a The TMA cohort (cohort two) was subject to IHC staining for both ALKBH5 and LYPD1. Representative images of higher or lower ALKBH5 staining and corresponding LYPD1 staining were shown, respectively (scale bars, 50 μm; magnification, 100× and 400×); b IHC staining statistics showed the percentage of HCC samples displaying higher or lower ALKBH5 levels and corresponding LYPD1 expression. For the same specimens, the IHC intensity of ALKBH5 and LYPD1 were frequently negatively correlated. c GEO data analysis of two HCC cohorts (GSE6764 and GSE3500) showed the inverse correlation of ALKBH5 and LYPD1 based on RNA expression; d A schematic illustration was proposed to summarize our findings about ALKHB5-guided m6A modulation on LYPD1 (the green and red colors indicated the activated and inhibited status, respectively). In brief, ALKBH5 is down-regulated in HCC cells compared with normal liver cells. Deficiency of ALKBH5 leads to an elevated m6A level of LYPD1 which is recognized and strengthened by the m6A effector IGF2BP1, thus reinforcing the expression of LYPD1. Accumulated LYPD1 promotes the proliferation and invasion capabilities of HCC cells, and further drives the tumorigenesis of HCC

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