The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression

Immune checkpoint inhibitors (ICIs) are extremely effective in a subgroup of mismatch repair-deficient (MMRd) cancers, but ∼50% remain resistant to treatment. We have shown for the first time that this may be due to the differential regulation of factors linked to response to ICIs upon loss of the d...

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Main Authors: Kirsten Brooksbank, Charlotte Smith, Eleni Maniati, Amy Gibson, Wai Yiu Tse, Amy Kate Hall, Jun Wang, Tyson V Sharp, Sarah A Martin
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:Neoplasia: An International Journal for Oncology Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S1476558625000879
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author Kirsten Brooksbank
Charlotte Smith
Eleni Maniati
Amy Gibson
Wai Yiu Tse
Amy Kate Hall
Jun Wang
Tyson V Sharp
Sarah A Martin
author_facet Kirsten Brooksbank
Charlotte Smith
Eleni Maniati
Amy Gibson
Wai Yiu Tse
Amy Kate Hall
Jun Wang
Tyson V Sharp
Sarah A Martin
author_sort Kirsten Brooksbank
collection DOAJ
description Immune checkpoint inhibitors (ICIs) are extremely effective in a subgroup of mismatch repair-deficient (MMRd) cancers, but ∼50% remain resistant to treatment. We have shown for the first time that this may be due to the differential regulation of factors linked to response to ICIs upon loss of the different MMR genes. Here, we show that increased PD-L1 expression is observed upon loss of the MMR genes MLH1, MSH2 and PMS2. However, this is not true upon loss of MSH6, and we show that this is due to a novel role for MSH6 as a direct regulator of PD-L1 transcription, dependent on recruitment by the histone trimethyltransferase SETD2. Next-generation sequencing of MLH1 and MSH6 knockout (KO) cells revealed that MSH6 KO cells have significantly lower microsatellite instability in comparison to MLH1 KO cells, despite MSH6 KO cells having a higher mutational burden. These findings emphasise the need for gene-specific stratification in the MMRd cohort.
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institution Kabale University
issn 1476-5586
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publishDate 2025-09-01
publisher Elsevier
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series Neoplasia: An International Journal for Oncology Research
spelling doaj-art-c9edfd0a554142258e66ea86bf0990892025-08-20T03:58:41ZengElsevierNeoplasia: An International Journal for Oncology Research1476-55862025-09-016710120710.1016/j.neo.2025.101207The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expressionKirsten Brooksbank0Charlotte Smith1Eleni Maniati2Amy Gibson3Wai Yiu Tse4Amy Kate Hall5Jun Wang6Tyson V Sharp7Sarah A Martin8Centre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Genomics & Computational Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Genomics & Computational Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UKCentre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK; Corresponding authors.Centre for Cancer Cell & Molecular Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK; Corresponding authors.Immune checkpoint inhibitors (ICIs) are extremely effective in a subgroup of mismatch repair-deficient (MMRd) cancers, but ∼50% remain resistant to treatment. We have shown for the first time that this may be due to the differential regulation of factors linked to response to ICIs upon loss of the different MMR genes. Here, we show that increased PD-L1 expression is observed upon loss of the MMR genes MLH1, MSH2 and PMS2. However, this is not true upon loss of MSH6, and we show that this is due to a novel role for MSH6 as a direct regulator of PD-L1 transcription, dependent on recruitment by the histone trimethyltransferase SETD2. Next-generation sequencing of MLH1 and MSH6 knockout (KO) cells revealed that MSH6 KO cells have significantly lower microsatellite instability in comparison to MLH1 KO cells, despite MSH6 KO cells having a higher mutational burden. These findings emphasise the need for gene-specific stratification in the MMRd cohort.http://www.sciencedirect.com/science/article/pii/S1476558625000879Mismatch repairMSH6Transcription factorPD-L1Immunotherapy
spellingShingle Kirsten Brooksbank
Charlotte Smith
Eleni Maniati
Amy Gibson
Wai Yiu Tse
Amy Kate Hall
Jun Wang
Tyson V Sharp
Sarah A Martin
The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression
Neoplasia: An International Journal for Oncology Research
Mismatch repair
MSH6
Transcription factor
PD-L1
Immunotherapy
title The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression
title_full The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression
title_fullStr The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression
title_full_unstemmed The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression
title_short The DNA mismatch repair protein, MSH6 is a novel regulator of PD-L1 expression
title_sort dna mismatch repair protein msh6 is a novel regulator of pd l1 expression
topic Mismatch repair
MSH6
Transcription factor
PD-L1
Immunotherapy
url http://www.sciencedirect.com/science/article/pii/S1476558625000879
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