SSX1 participates in a transformation-related mechanism involving cytidine deaminase CDA activity with inputs from oncogenes and DNA damage repair machinery.
Abstract
We describe a series of transcriptional responses to expression of a chromatin modifying enzyme from the SSX family. Expression of the carboxy terminus of SSX1 resulted in activation of the cytidine deaminase CDA without a similar change in expression of GDA. SSX1 activation resulted in induction of the oncogene PIM1. The UL16 binding protein ULBP1 was a major molecular target of SSX1; SSX1 silenced ULBP3. The inka box actin regulator 2 INKA2 was a second major SSX1 molecular target. MLLT11 was activated by SSX1 concomitant with induction of DDIT family damage signaling genes. SSX1 activation silenced the transcriptional elongator TCEA3. SSX1 activated expression of the H2.0 like homeobox HLX but silenced Sox9 while activating the tumor suppressor p53. SSX1 has functions in a cytidine deamination process related to transinformation, controls expression of basic oncogenes and homeoboxes, interacts with epigenetic chromatin regulators and participates in functions at the DNA including transcriptional elongation.
Fields of Study & Subjects
Epigenetics and DNA Methylation
Genomics and Chromatin Dynamics
Chromatin Remodeling and Cancer
Publication details
- Journal / source
- Zenodo (CERN European Organization for Nuclear Research)
- Publication date
- 17 January 2026
- Document type
- Preprint