SSX1 participates in a transformation-related mechanism involving cytidine deaminase CDA activity with inputs from oncogenes and DNA damage repair machinery.

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Authors: Shahan Mamoor
Cited by: 0

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