Figure 6

Differential transcriptome analysis of LN-229 KO cell clones and LN-428 OE cell population. (A and B) Gene ontology analysis indicating the most enriched pathways for the significantly altered genes in the modified cell lines, defined by STRING database. (C and D) Heat-maps indicating the shortlisted genes which are most significantly modulated under both comparative conditions. (E and F) Validation of gene expression by qRT-PCR. CHD7 is indicated in red. Down-regulated (black) and up-regulated (blue) genes related to tumorigenesis, cell migration or cell invasion. Values are the means ± SEM (n = 3, ^*p < 0.05, ^**p < 0.01, ^***p < 0.001; Student’s t-test). (G) Proposed model for CHD7 regulation of glioblastoma cell motility and invasiveness. CHD7 is recruited to binding sites through interactions with cell type-specific transcription factors (TFs) and histone modifications. The energy provided by ATP hydrolysis enables nucleosome translocation revealing extra TF-binding sites (yellow rectangle). Binding of additional TFs, associated with co-activators, promotes DNA accessibility favoring transcription. In glioblastoma cells, CHD7 modulates the expression of several adhesion molecules, such as integrins and cadherins, stimulating cell motility and invasiveness.