Loss of Rnf43 Accelerates Kras-Mediated Neoplasia and Remodels the Tumor Immune Microenvironment in Pancreatic Adenocarcinoma.


Journal

Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630

Informations de publication

Date de publication:
04 2022
Historique:
received: 03 06 2021
revised: 22 11 2021
accepted: 22 12 2021
pubmed: 2 1 2022
medline: 3 5 2022
entrez: 1 1 2022
Statut: ppublish

Résumé

RNF43 is an E3 ubiquitin ligase that is recurrently mutated in pancreatic ductal adenocarcinoma (PDAC) and precursor cystic neoplasms of the pancreas. The impact of RNF43 mutations on PDAC is poorly understood and autochthonous models have not been characterized sufficiently. In this study, we describe a genetically engineered mouse model (GEMM) of PDAC with conditional expression of oncogenic Kras and deletion of the catalytic domain of Rnf43 in exocrine cells. We generated Ptf1a-Cre;LSL-KrasG12D;Rnf43 We demonstrate that KRC mice display a marked increase in incidence of high-grade cystic lesions of the pancreas and PDAC compared with KC. Importantly, KRC mice have a significantly decreased survival compared with KC mice. Using single-cell RNA sequencing, we demonstrated that KRC tumor progression is accompanied by a decrease in macrophages, as well as an increase in T and B lymphocytes, with evidence of increased immune checkpoint molecule expression and affinity maturation, respectively. This was in stark contrast to the tumor immune microenvironment observed in the KPC PDAC GEMM. Furthermore, expression of the chemokine CXCL5 was found to be specifically decreased in KRC cancer cells by means of epigenetic regulation and emerged as a putative candidate for mediating the unique KRC immune landscape. The KRC GEMM establishes RNF43 as a bona fide tumor suppressor gene in PDAC. This GEMM features a markedly different immune microenvironment compared with previously reported PDAC GEMMs and puts forth a rationale for an immunotherapy approach in this subset of PDAC cases.

Sections du résumé

BACKGROUND & AIMS
RNF43 is an E3 ubiquitin ligase that is recurrently mutated in pancreatic ductal adenocarcinoma (PDAC) and precursor cystic neoplasms of the pancreas. The impact of RNF43 mutations on PDAC is poorly understood and autochthonous models have not been characterized sufficiently. In this study, we describe a genetically engineered mouse model (GEMM) of PDAC with conditional expression of oncogenic Kras and deletion of the catalytic domain of Rnf43 in exocrine cells.
METHODS
We generated Ptf1a-Cre;LSL-KrasG12D;Rnf43
RESULTS
We demonstrate that KRC mice display a marked increase in incidence of high-grade cystic lesions of the pancreas and PDAC compared with KC. Importantly, KRC mice have a significantly decreased survival compared with KC mice. Using single-cell RNA sequencing, we demonstrated that KRC tumor progression is accompanied by a decrease in macrophages, as well as an increase in T and B lymphocytes, with evidence of increased immune checkpoint molecule expression and affinity maturation, respectively. This was in stark contrast to the tumor immune microenvironment observed in the KPC PDAC GEMM. Furthermore, expression of the chemokine CXCL5 was found to be specifically decreased in KRC cancer cells by means of epigenetic regulation and emerged as a putative candidate for mediating the unique KRC immune landscape.
CONCLUSIONS
The KRC GEMM establishes RNF43 as a bona fide tumor suppressor gene in PDAC. This GEMM features a markedly different immune microenvironment compared with previously reported PDAC GEMMs and puts forth a rationale for an immunotherapy approach in this subset of PDAC cases.

Identifiants

pubmed: 34973294
pii: S0016-5085(21)04169-X
doi: 10.1053/j.gastro.2021.12.273
pmc: PMC8934289
mid: NIHMS1767845
pii:
doi:

Substances chimiques

RNF43 protein, mouse EC 2.3.2.27
Ubiquitin-Protein Ligases EC 2.3.2.27
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1303-1318.e18

Subventions

Organisme : NCI NIH HHS
ID : P30 CA016672
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA221707
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA218004
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA220236
Pays : United States

Informations de copyright

Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Auteurs

Abdel Nasser Hosein (AN)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas; Department of Internal Medicine, Division of Hematology and Oncology, The University of Texas Southwestern Medical Center, Dallas, Texas; Advocate Aurora Health, Vince Lombardi Cancer Clinic, Sheboygan, Wisconsin.

Gita Dangol (G)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Takashi Okumura (T)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Jason Roszik (J)

Department of Melanoma Medical Oncology Research, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Kimal Rajapakshe (K)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Megan Siemann (M)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Mohamed Zaid (M)

Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Bidyut Ghosh (B)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Maria Monberg (M)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Paola A Guerrero (PA)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Aatur Singhi (A)

Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.

Cara L Haymaker (CL)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Hans Clevers (H)

Oncode Institute, Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences, University Medical Center Utrecht and Princess Maxima Center, Utrecht, the Netherlands.

Lotfi Abou-Elkacem (L)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Sonja M Woermann (SM)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Anirban Maitra (A)

Department of Translational Molecular Pathology, Ahmad Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas. Electronic address: amaitra@mdanderson.org.

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Classifications MeSH