JUN

Overview

JUN (Jun Proto-Oncogene, AP-1 Transcription Factor Subunit) encodes a component of the AP-1 transcription factor complex. In cancer genomics, JUN is recurrently amplified in dedifferentiated liposarcoma (DDLPS) where it functions as an adipocyte-differentiation inhibitor and defines the poor-prognosis K1 molecular subtype, making it a proposed therapeutic target.

Alterations observed in the corpus

  • Amplification in DDLPS (42%): JUN amplification defines the poor-prognosis K1 SCNA cluster in DDLPS (n=50, TCGA SARC); JUN and PTPRQ amplifications were nearly mutually exclusive (p=0.026). PMID:29100075
  • Adipocyte-differentiation-inhibitor function: JUN is one of five adipocyte-differentiation-inhibitor amplifications in DDLPS (alongside DDIT3 32%, PTPRQ 46%, YAP1 16%, CEBPA 24%), contributing to the block in terminal differentiation. PMID:29100075
  • Identified as novel recurrently mutated gene in metastatic colorectal cancer in a 1,211-patient WES/WGS/transcriptome study PMID:29316426

Cancer types (linked)

  • Dedifferentiated Liposarcoma (DDLS): JUN amplification at 42% frequency defines the K1 SCNA subtype with the worst disease-specific survival (combined with hypermethylation in K1+K2-hypermethylated group: HR=4.4, p=0.002 vs Meth1). PMID:29100075

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • JUN amplification in the poor-prognosis K1 DDLPS cluster is proposed as a tractable target as JUN inhibitors mature; no clinical-stage JUN inhibitor data are reported in this corpus. PMID:29100075

Open questions

  • Clinical efficacy of JUN inhibitors in JUN-amplified DDLPS is unvalidated; these recommendations are hypothesis-generating from the TCGA SARC cohort. PMID:29100075

Sources

This page was processed by crosslinker on 2026-05-15. - PMID:29316426

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