SSX addiction in melanoma propagates tumor growth and metastasis

Sofie Traynor, Malene Laage Ebstrup, Odd Lilleng Gammelgaard, Behzad Mansoori, Mikkel Green Terp, Cecilie Rose Hauge Rein, Sofie Rattenborg, Christina Bøg Pedersen, Henrik Jørn Ditzel, Morten Frier Gjerstorff*

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

22 Downloads (Pure)


Cancer/testis antigens are receiving attention as targets for cancer therapy due to their germ- and cancer cell-restricted expression. However, many of these antigens are inconsistently expressed among cancer types and individual tumors. Here, we show that members of the SSX cancer/testis antigen family comprise attractive targets in the majority of melanoma patients, as SSX is expressed in more than 90% of primary melanomas and metastases and plays a critical role in metastatic progression. Accordingly, SSX silencing in melanoma mouse xenograft models reduced tumor growth and completely abolished the formation of metastatic lesions in lungs and livers. Mechanistically, we demonstrate that silencing SSX in melanoma cells induces cell cycle S-phase stalling, leading to proliferative arrest and enhanced apoptosis, which elucidates the inhibitory effect of SSX loss on tumor growth and colonization capacity. Silencing SSX further compromised the capacity of melanoma cells to migrate and invade, influencing these cells’ capability to spread and colonize. Taken together, these studies highlight SSX proteins as pivotal targets in melanoma with implications for blocking metastatic progression.

Original languageEnglish
Article number998000
JournalFrontiers in Oncology
Number of pages11
Publication statusPublished - 7. Oct 2022

Bibliographical note

Publisher Copyright:
Copyright © 2022 Traynor, Ebstrup, Gammelgaard, Mansoori, Terp, Rein, Rattenborg, Pedersen, Ditzel and Gjerstorff.


  • cancer/testis antigen (CTA)
  • cell cycle arrest
  • melanoma
  • metastasis
  • SSX


Dive into the research topics of 'SSX addiction in melanoma propagates tumor growth and metastasis'. Together they form a unique fingerprint.

Cite this