ANKRD10

ANKRD10 is regulated at the level of alternative splicing by the RNA-binding protein RBPMS, and its splice isoform ANKRD10-2 functions as a transcriptional co-activator of MYC in bladder cancer (PMID:40044952). Depletion of RBPMS shifts splicing toward the ANKRD10-2 isoform, which augments MYC transcriptional activity and drives cancer cell migration and invasion (PMID:40044952). Beyond this RBPMS–ANKRD10-2–MYC axis, no further mechanistic detail for ANKRD10 has been characterized in the available corpus.

1. 2025 Medium

   Established that ANKRD10 is a splicing target of RBPMS and that its ANKRD10-2 isoform acts as a MYC co-activator promoting bladder cancer invasiveness, placing ANKRD10 downstream of an RNA-binding regulator and upstream of MYC-driven transcription.

   Evidence RNA-Seq identification of ANKRD10 as an RBPMS splicing target, with RBPMS and ANKRD10-2 knockdown plus migration/invasion and MYC transcriptional activity assays in bladder cancer cells

   PMID:40044952

   Open questions at the time

   • Mechanism by which ANKRD10-2 physically co-activates MYC (direct binding vs. indirect) is not defined
   • No structural or domain-level basis for isoform-specific co-activator activity
   • Findings from a single lab and limited to bladder cancer context

• Whether ANKRD10 has functions outside the RBPMS–MYC axis, and the molecular activity and localization of its protein product, remain unknown.
• No biochemical characterization of ANKRD10 protein interactions or domains
• No subcellular localization data
• No evidence in tissues or cancers other than bladder