SMARCD1 subunit of SWI/SNF chromatin remodeling complexes collaborates with p53 to exert an oncogenic role in B-ALL by maintaining high metabolic activity
Observations indicate that p53 enhances survival and proliferation in B-ALL, suggesting therapeutic avenues targeting chromatin remodeling and metabolic pathways.
Key Points
This research aims to elucidate the role of SMARCD1 in cooperation with p53 in B-ALL.
Investigated cellular proliferation and survival after SMARCD1 and TP53 inactivation in B-ALL cell lines and PDX cells.
Utilized co-immunoprecipitation and bimolecular fluorescence complementation to explore interactions between SMARCD1 and p53.
Performed bulk RNA sequencing to identify gene expression changes and pathways affected by the loss of SMARCD1 or p53.
SMARCD1 inactivation led to defects in cellular proliferation and survival of B-ALL cells.
Co-depletion of SMARCD1 and p53 did not rescue proliferation defects, indicating their cooperative role.
RNA sequencing revealed downregulation of pathways linked to metabolism and survival, including hypoxia and fatty acid metabolism.