Co-Regulation of Immune Checkpoint PD-L1 with Interferon-Gamma Signaling is Associated with a Survival Benefit in Renal Cell Cancer.


Journal

Targeted oncology
ISSN: 1776-260X
Titre abrégé: Target Oncol
Pays: France
ID NLM: 101270595

Informations de publication

Date de publication:
06 2020
Historique:
pubmed: 5 6 2020
medline: 3 3 2021
entrez: 5 6 2020
Statut: ppublish

Résumé

Programmed death ligand (PD-L1)-based immune checkpoint blockade therapy for metastatic renal cell carcinoma (RCC) achieves significant response rates in a subgroup of patients. The relevance of PD-L1 gene regulation for disease outcome is not clear. To evaluate PD-L1 expression and its dependence on interferon-γ (IFN-γ) in RCC cell lines and tissues in relation to disease outcome. Regulation of PD-L1-mRNA and PD-L1 protein was studied in cell lines from clear cell RCC (ccRCC) and papillary RCC (pRCC) by quantitative RT-PCR and Western-blot analysis. PD-L1-mRNA correlation and gene-set enrichment analysis (GSEA) of the IFN-γ pathway were conducted with RNA-Seq from ccRCC, pRCC, and skin cutaneous melanoma (SKCM) tissue. In addition, patient overall survival (OS) and disease-free survival (DFS) (cBioPortal for Cancer Genomics) were considered. In ccRCC-like cell lines, PD-L1 was induced by canonical IFN-γ signaling, whereas in a pRCC-like cell line, PD-L1 was refractory towards IFN-γ signaling. In ccRCC and SKCM tissues, GSEA revealed significant IFN-γ pathway activation in tissue samples with high PD-L1-mRNA levels. This was not observed in pRCC tissue. ccRCC and SKMC patients with low PD-L1-mRNA levels had significantly shorter OS and DFS than those with high PD-L1-mRNA levels. In pRCC patients, no significant difference in OS and DFS with regard to PD-L1-mRNA tissue levels was obvious. The findings suggest that ccRCC and pRCC differ with respect to PD-L1 regulation by IFN-γ-signaling. High PD-L1-mRNA levels in tumor tissues with a positive IFN-γ signature favorably affect OS and DFS.

Sections du résumé

BACKGROUND
Programmed death ligand (PD-L1)-based immune checkpoint blockade therapy for metastatic renal cell carcinoma (RCC) achieves significant response rates in a subgroup of patients. The relevance of PD-L1 gene regulation for disease outcome is not clear.
OBJECTIVE
To evaluate PD-L1 expression and its dependence on interferon-γ (IFN-γ) in RCC cell lines and tissues in relation to disease outcome.
METHODS AND PATIENTS
Regulation of PD-L1-mRNA and PD-L1 protein was studied in cell lines from clear cell RCC (ccRCC) and papillary RCC (pRCC) by quantitative RT-PCR and Western-blot analysis. PD-L1-mRNA correlation and gene-set enrichment analysis (GSEA) of the IFN-γ pathway were conducted with RNA-Seq from ccRCC, pRCC, and skin cutaneous melanoma (SKCM) tissue. In addition, patient overall survival (OS) and disease-free survival (DFS) (cBioPortal for Cancer Genomics) were considered.
RESULTS
In ccRCC-like cell lines, PD-L1 was induced by canonical IFN-γ signaling, whereas in a pRCC-like cell line, PD-L1 was refractory towards IFN-γ signaling. In ccRCC and SKCM tissues, GSEA revealed significant IFN-γ pathway activation in tissue samples with high PD-L1-mRNA levels. This was not observed in pRCC tissue. ccRCC and SKMC patients with low PD-L1-mRNA levels had significantly shorter OS and DFS than those with high PD-L1-mRNA levels. In pRCC patients, no significant difference in OS and DFS with regard to PD-L1-mRNA tissue levels was obvious.
CONCLUSIONS
The findings suggest that ccRCC and pRCC differ with respect to PD-L1 regulation by IFN-γ-signaling. High PD-L1-mRNA levels in tumor tissues with a positive IFN-γ signature favorably affect OS and DFS.

Identifiants

pubmed: 32495158
doi: 10.1007/s11523-020-00728-8
pii: 10.1007/s11523-020-00728-8
pmc: PMC7283197
doi:

Substances chimiques

B7-H1 Antigen 0
CD274 protein, human 0
Immune Checkpoint Inhibitors 0
Interferon-gamma 82115-62-6

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

377-390

Références

Cancer Immunol Immunother. 2018 Mar;67(3):403-412
pubmed: 29150702
In Vivo. 2000 May-Jun;14(3):393-400
pubmed: 10904872
Int J Mol Sci. 2017 Jun 21;18(6):
pubmed: 28635644
Signal Transduct Target Ther. 2018 Sep 28;3:26
pubmed: 30275987
Nat Rev Clin Oncol. 2019 Mar;16(3):151-167
pubmed: 30523282
N Engl J Med. 2019 Mar 21;380(12):1116-1127
pubmed: 30779529
Cancer Discov. 2017 Feb;7(2):188-201
pubmed: 27903500
Nat Genet. 2003 Jul;34(3):267-73
pubmed: 12808457
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50
pubmed: 16199517
N Engl J Med. 2019 Mar 21;380(12):1103-1115
pubmed: 30779531
Mol Cancer. 2016 Dec 19;15(1):83
pubmed: 27993170
Sci Signal. 2013 Apr 02;6(269):pl1
pubmed: 23550210
N Engl J Med. 2015 Jan 22;372(4):311-9
pubmed: 25482239
Cell. 2017 Feb 9;168(4):707-723
pubmed: 28187290
Proc Natl Acad Sci U S A. 2011 Jan 25;108(4):1439-44
pubmed: 21220347
Science. 2018 Feb 16;359(6377):801-806
pubmed: 29301960
Nature. 1985 Jun 20-26;315(6021):672-6
pubmed: 3925348
Oncotarget. 2015 May 30;6(15):13506-19
pubmed: 25940795
Cancer Res. 2007 Apr 1;67(7):3171-6
pubmed: 17409424
Cancer Res. 2015 Jun 1;75(11):2139-45
pubmed: 25977340
J Exp Med. 1998 Mar 16;187(6):875-83
pubmed: 9500790
Curr Opin Immunol. 2014 Apr;27:16-25
pubmed: 24531241
N Engl J Med. 2018 Apr 05;378(14):1277-1290
pubmed: 29562145
Clin Cancer Res. 2015 Mar 1;21(5):1071-7
pubmed: 25538263
Cancer Discov. 2012 May;2(5):401-4
pubmed: 22588877
Cell. 2016 Dec 1;167(6):1540-1554.e12
pubmed: 27912061
Immunity. 2017 Dec 19;47(6):1007-1009
pubmed: 29262340
Onco Targets Ther. 2018 Oct 04;11:6505-6524
pubmed: 30323625
J Clin Oncol. 2015 Mar 20;33(9):983-91
pubmed: 25534375
Br J Cancer. 2015 Apr 28;112(9):1421-7
pubmed: 25856776
Cell Rep. 2017 May 9;19(6):1189-1201
pubmed: 28494868
Immunity. 2017 Dec 19;47(6):1083-1099.e6
pubmed: 29246442
Pathol Oncol Res. 2020 Apr;26(2):651-663
pubmed: 31748880
Nat Med. 2018 Jun;24(6):749-757
pubmed: 29867230
J Immunol. 2009 Feb 1;182(3):1325-33
pubmed: 19155478
Nature. 2017 Sep 7;549(7670):101-105
pubmed: 28813417
Nat Commun. 2017 May 10;8:15165
pubmed: 28489074
J Biol Chem. 2017 Dec 15;292(50):20683-20693
pubmed: 29066622
Cancer Gene Ther. 2001 Jul;8(7):529-36
pubmed: 11498775
Cell. 2016 Oct 6;167(2):397-404.e9
pubmed: 27667683
N Engl J Med. 2016 Sep 1;375(9):819-29
pubmed: 27433843
Eur Urol. 2019 Aug;76(2):151-156
pubmed: 31151678

Auteurs

Jörg Hänze (J)

Department of Urology and Pediatric Urology, Faculty of Medicine, Philipps-University Marburg, 35043, Baldingerstraße Marburg, Germany. haenze@staff.uni-marburg.de.

Moritz Wegner (M)

Department of Urology and Pediatric Urology, Faculty of Medicine, Philipps-University Marburg, 35043, Baldingerstraße Marburg, Germany.

Elfriede Noessner (E)

Immunoanalytics Research Group Tissues Control of Immunocytes, Helmholtz Zentrum München, National Research Center for Environmental Health, Munich, Germany.

Rainer Hofmann (R)

Department of Urology and Pediatric Urology, Faculty of Medicine, Philipps-University Marburg, 35043, Baldingerstraße Marburg, Germany.

Axel Hegele (A)

Department of Urology and Pediatric Urology, Faculty of Medicine, Philipps-University Marburg, 35043, Baldingerstraße Marburg, Germany.

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Classifications MeSH