Inhibition of MER proto-oncogene tyrosine kinase by an antisense oligonucleotide enhances treatment efficacy of immunoradiotherapy.

Antisense oligonucleotide Antitumor immune response Immunoradiotherapy Immunotherapy resistance M1 macrophage MerTK

Journal

Journal of experimental & clinical cancer research : CR
ISSN: 1756-9966
Titre abrégé: J Exp Clin Cancer Res
Pays: England
ID NLM: 8308647

Informations de publication

Date de publication:
06 Mar 2024
Historique:
received: 22 01 2024
accepted: 21 02 2024
medline: 6 3 2024
pubmed: 6 3 2024
entrez: 5 3 2024
Statut: epublish

Résumé

The combination of radiotherapy and immunotherapy (immunoradiotherapy) has been increasingly used for treating a wide range of cancers. However, some tumors are resistant to immunoradiotherapy. We have previously shown that MER proto-oncogene tyrosine kinase (MerTK) expressed on macrophages mediates resistance to immunoradiotherapy. We therefore sought to develop therapeutics that can mitigate the negative impact of MerTK. We designed and developed a MerTK specific antisense oligonucleotide (ASO) and characterized its effects on eliciting an anti-tumor immune response in mice. 344SQR cells were injected into the right legs on day 0 and the left legs on day 4 of 8-12 weeks old female 129sv/ev mice to establish primary and secondary tumors, respectively. Radiation at a dose of 12 Gy was given to the primary tumors on days 8, 9, and 10. Mice received either anti-PD-1, anti-CTLA-4 or/and MerTK ASO starting from day 1 post tumor implantation. The composition of the tumor microenvironment and the level of MerTK on macrophages in the tumor were evaluted by flow cytometry. The expression of immune-related genes was investigated with NanoString. Lastly, the impact of MerTK ASO on the structure of the eye was histologically evaluated. Remarkably, the addition of MerTK ASO to XRT+anti-PD1 and XRT+anti-CTLA4 profoundly slowed the growth of both primary and secondary tumors and significantly extended survival. The ASO significantly reduced the expression of MerTK in tumor-associated macrophages (TAMs), reprograming their phenotype from M2 to M1. In addition, MerTK ASO increased the percentage of Granzyme B The MerTK ASO can significantly downregulate the expression of MerTK on TAMs, thereby promoting antitumor immune response. The combination of MerTK ASO with immunoradiotherapy can safely and significantly slow tumor growth and improve survival.

Sections du résumé

BACKGROUND BACKGROUND
The combination of radiotherapy and immunotherapy (immunoradiotherapy) has been increasingly used for treating a wide range of cancers. However, some tumors are resistant to immunoradiotherapy. We have previously shown that MER proto-oncogene tyrosine kinase (MerTK) expressed on macrophages mediates resistance to immunoradiotherapy. We therefore sought to develop therapeutics that can mitigate the negative impact of MerTK. We designed and developed a MerTK specific antisense oligonucleotide (ASO) and characterized its effects on eliciting an anti-tumor immune response in mice.
METHODS METHODS
344SQR cells were injected into the right legs on day 0 and the left legs on day 4 of 8-12 weeks old female 129sv/ev mice to establish primary and secondary tumors, respectively. Radiation at a dose of 12 Gy was given to the primary tumors on days 8, 9, and 10. Mice received either anti-PD-1, anti-CTLA-4 or/and MerTK ASO starting from day 1 post tumor implantation. The composition of the tumor microenvironment and the level of MerTK on macrophages in the tumor were evaluted by flow cytometry. The expression of immune-related genes was investigated with NanoString. Lastly, the impact of MerTK ASO on the structure of the eye was histologically evaluated.
RESULTS RESULTS
Remarkably, the addition of MerTK ASO to XRT+anti-PD1 and XRT+anti-CTLA4 profoundly slowed the growth of both primary and secondary tumors and significantly extended survival. The ASO significantly reduced the expression of MerTK in tumor-associated macrophages (TAMs), reprograming their phenotype from M2 to M1. In addition, MerTK ASO increased the percentage of Granzyme B
CONCLUSIONS CONCLUSIONS
The MerTK ASO can significantly downregulate the expression of MerTK on TAMs, thereby promoting antitumor immune response. The combination of MerTK ASO with immunoradiotherapy can safely and significantly slow tumor growth and improve survival.

Identifiants

pubmed: 38443968
doi: 10.1186/s13046-024-02992-2
pii: 10.1186/s13046-024-02992-2
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

70

Informations de copyright

© 2024. The Author(s).

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Auteurs

Yun Hu (Y)

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

Alexey Revenko (A)

Ionis Pharmaceuticals, Carlsbad, CA, 92008, USA.

Hampartsoum Barsoumian (H)

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

Genevieve Bertolet (G)

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

Natalie Wall Fowlkes (NW)

Department of Veterinary Medicine & Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Hadi Maazi (H)

Ionis Pharmaceuticals, Carlsbad, CA, 92008, USA.

Morgan Maureen Green (MM)

Department of Veterinary Medicine & Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Kewen He (K)

Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China.

Duygu Sezen (D)

Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Department of Radiation Oncology, Koc University School of Medicine, Istanbul, Turkey.

Tiffany A Voss (TA)

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

Claudia S Kettlun Leyton (CSK)

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

Fatemeh Masrorpour (F)

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

Zahid Rafiq (Z)

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

Nahum Puebla-Osorio (N)

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

Carola Leuschner (C)

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

Robert MacLeod (R)

Ionis Pharmaceuticals, Carlsbad, CA, 92008, USA.

Maria Angelica Cortez (MA)

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

James W Welsh (JW)

Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA. Jwelsh@mdanderson.org.

Classifications MeSH