Fig. 7. CHD1L-ZKSCAN3 axis promotes HCC migration partially through autophagic degradation of Paxillin.

A Co-IP assays of interaction between LC3B and Paxillin in QGY-7703 cells. The precipitates were examined with anti-Paxillin and anti-LC3B antibodies, respectively. B WB analysis for Paxillin accumulation in QGY-7703 cells treated with Sreamble or shRNA for ATG5. C Immunofluorescence of FA proteins Paxillin and Zyxin in control and ATG5 silencing cells. Scale bars: 10 μM. D WB analysis for Paxillin accumulation in QGY-7703 cells treated with or without Dox. E Immunofluorescence of FA proteins Paxillin and Zyxin in QGY-7703 cell with or without Dox inducing. Scale bars represent as shown. F Paxillin accumulation defects in CHD1L-depleted cells in response to ZKSCAN3 knockdown. Images/immunoblots are representative of three independent experiments. G The mRNA and protein level of Paxillin was analyzed in QGY-7703 cells treated with the most efficient siRNA fragment for Paxillin (hereafter referred to as si-Paxillin), compared with the scrambled control. H QGY-7703 cells with Dox treated were subjected to wound-healing assay and migration in response to Paxillin knockdown, compared with the scrambled control. Quantification of migration indicated group (****p < 0.0001, Student t test; values are shown as mean ± SD calculated from three parallel experiments; n = 5). Scale bar as indicated.