Fig. 2: CHD1L promotes autophagy in HCC.
From: CHD1L augments autophagy-mediated migration of hepatocellular carcinoma through targeting ZKSCAN3
A Enrichment of the gene ontology (GO) terms of differential mRNAs in CHD1L- vs vector-QGY-7703 clones. B Performance of GSEA based on the differential genes in CHD1L- vs vector-QGY-7703 clones. Enrichment analysis was performed on the indicated gene sets. C Correlation plots show expression of indicated genes and CHD1L in 469 primary HCC tumor and para-tumor samples analyzed using RNA-sequencing in TCGA. D Bright light and immunofluorescence for endogenous LC3B images of patient-derived organoid (PDOs) established from HCC. Cystic PDO structures were recognized starting on day 6. Bar was as indicated, quantification of LC3B puncta per cell for Vector or forced CHD1L group. (**p < 0.01; Student’s t test; Mean ± SD, n = 10/group). E WB analysis for changes in LC3 conversion and P62 level affected by overexpression of CHD1L in the presence or absence of 80 nM Baf A1 (6 h). The QGY-7703 cells were transiently transfected with GFP-tagged CHD1L expressing constructs or the control vector. LC3-I, non-lipidated LC3; LC3-II, lipidated LC3. The β-actin protein was as a loading control. F WB analysis for changes in LC3 conversion and P62 level affected by CHD1L-deficient in the presence or absence of 80 nM bafA1 (6 h) in Huh7 and QGY-7703-iKO cells. G Representative IHC images for the expression of CHD1L and LC3B in primary HCC tumor.
