Titre
Overexpression of SMARCE1 is associated with CD8+ T-cell infiltration in early stage ovarian cancer.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Auteur(s)
Giannakakis, A.
Auteure/Auteur
Karapetsas, A.
Auteure/Auteur
Dangaj, D.
Auteure/Auteur
Lanitis, E.
Auteure/Auteur
Tanyi, J.
Auteure/Auteur
Coukos, G.
Auteure/Auteur
Sandaltzopoulos, R.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1878-5875
Statut éditorial
Publié
Date de publication
2014
Volume
53
Première page
389
Dernière page/numéro d’article
398
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Résumé
T-lymphocyte infiltration in ovarian tumors has been linked to a favorable prognosis, hence, exploring the mechanism of T-cell recruitment in the tumor is warranted. We employed a differential expression analysis to identify genes over-expressed in early stage ovarian cancer samples that contained CD8 infiltrating T-lymphocytes. Among other genes, we discovered that TTF1, a regulator of ribosomal RNA gene expression, and SMARCE1, a factor associated with chromatin remodeling were overexpressed in first stage CD8+ ovarian tumors. TTF1 and SMARCE1 mRNA levels showed a strong correlation with the number of intra-tumoral CD8+ cells in ovarian tumors. Interestingly, forced overexpression of SMARCE1 in SKOV3 ovarian cancer cells resulted in secretion of IL8, MIP1b and RANTES chemokines in the supernatant and triggered chemotaxis of CD8+ lymphocytes in a cell culture assay. The potency of SMARCE1-mediated chemotaxis appeared comparable to that caused by the transfection of the CXCL9 gene, coding for a chemokine known to attract T-cells. Our analysis pinpoints TTF1 and SMARCE1 as genes potentially involved in cancer immunology. Since both TTF1 and SMARCE1 are involved in chromatin remodeling, our results imply an epigenetic regulatory mechanism for T-cell recruitment that invites deciphering.
PID Serval
serval:BIB_3EE5F8B4AE65
PMID
Date de création
2014-09-19T16:07:48.474Z
Date de création dans IRIS
2025-05-20T19:24:41Z