Recently, Wan et al. [ xref ] have elucidated that EZH2-K348 residue is acetylated by acetyltransferase P300/CBP-associated factor (PCAF) and is deacetylated by deacetylase SIRT1 in lung cancer cells.

Because directional migration depends on the activation of small GTPases at the leading edge of cell protrusions and because Trio is a well-known GEF that likely acts upstream of the small GTPase family xref , xref , we evaluated whether Trio activated Rac1 and Cdc42 in NCC migration.

Desmoplastic small round cell tumor (DSRCT) is characterized by the EWSR1-WT1 t(11;22) (p13:q12) translocation.

EWSR1-WT1 fusions were noted to be simple, balanced events.

PDX models harbored the pathognomic EWSR1-WT1 fusion and were highly representative of corresponding tumors.

Six genes interacting with both EZH2 and NSD2 were further identified, that were cyclin A2 (CCNA2), cyclin dependent kinase 2 (CDK2), lysine demethylase 2B (KDM2B), kinesin family member 11 (KIF11), kinesin family member 23 (KIF23), and proliferating cell nuclear antigen (PCNA) ( xref ).

The interaction of EZH2 and NSD2 was illustrated in vitro in the proliferation, migration, and invasion of TNBC cells.

Thus, we next checked whether the binding of DDX11 and EZH2 may affect the ubiquitination of EZH2 in HCC cells.

Results demonstrated that the ubiquitination of EZH2 protein was obviously enhanced by the depletion of DDX11 ( xref ).

Thus, E2F1 and EZH2 formed a positive feedback loop to upregulate the expression of DDX11 in HCC cells.

Several studies demonstrated that EZH2 could interacted with E2F1 to enhance its transcriptional activity.

In our study, DDX11 interacted with EZH2 to enhance its protein stability by avoiding the ubiquitination-mediated protein degradation.

We next examined whether DDX11 bound to EZH2 in HCC cells.

Further studies reveal that DDX11 interacts with EZH2 in HCC cells to protect it from ubiquitination-mediated protein degradation, consequently resulting in the downregulation of p21.

Thus, we next checked whether the binding of DDX11 and EZH2 may affect the ubiquitination of EZH2 in HCC cells.

Fifty-eight B-other ALL patients (not BCR-ABL1 , KMT2A -rearranged, ETV6-RUNX1 , TCF3-PBX1 , or iAMP21) were included in the study.