Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer

Abstract SET domain bifurcated histone lysine methyltransferase 1 (SETDB1/ESET), a pivotal H3K9 methyltransferase, has been extensively studied since its discovery over two decades ago. SETDB1 plays critical roles in immune regulation, including B cell maturation, T‐cell activity modulation, and end...

Full description

Saved in:
Bibliographic Details
Main Authors: Bo‐Syong Pan, Cheng‐Yu Lin, Gilbert Aaron Lee, Hui‐Kuan Lin
Format: Article
Language:English
Published: Wiley 2025-03-01
Series:Kaohsiung Journal of Medical Sciences
Subjects:
Online Access:https://doi.org/10.1002/kjm2.12933
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850035376008200192
author Bo‐Syong Pan
Cheng‐Yu Lin
Gilbert Aaron Lee
Hui‐Kuan Lin
author_facet Bo‐Syong Pan
Cheng‐Yu Lin
Gilbert Aaron Lee
Hui‐Kuan Lin
author_sort Bo‐Syong Pan
collection DOAJ
description Abstract SET domain bifurcated histone lysine methyltransferase 1 (SETDB1/ESET), a pivotal H3K9 methyltransferase, has been extensively studied since its discovery over two decades ago. SETDB1 plays critical roles in immune regulation, including B cell maturation, T‐cell activity modulation, and endogenous retrovirus (ERV) silencing. While essential for normal immune cell function, SETDB1 overexpression in cancer cells disrupts immune responses by suppressing tumor immunogenicity and facilitating immune evasion. This is achieved through the repression of anti‐tumor immune cell production, ERV silencing, and interference with the type I interferon pathway leading to inhibiting immune checkpoint blockade (ICB) efficacy. Beyond its immunological implications, SETDB1 overexpression fosters tumor growth and metastasis via transcriptional silencing of tumor suppressor genes through histone regulation and activating oncogenic signaling by non‐histone regulation. These multifaceted roles make SETDB1 an attractive epigenetic target for novel cancer therapies. This review explores SETDB1's dual function in immune regulation and tumor progression, emphasizing its potential in the development of innovative cancer treatments targeting epigenetic dysregulation and oncogenic signaling.
format Article
id doaj-art-47a5cdf1b9cf401e9eb6eea7ad950d77
institution DOAJ
issn 1607-551X
2410-8650
language English
publishDate 2025-03-01
publisher Wiley
record_format Article
series Kaohsiung Journal of Medical Sciences
spelling doaj-art-47a5cdf1b9cf401e9eb6eea7ad950d772025-08-20T02:57:30ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502025-03-01413n/an/a10.1002/kjm2.12933Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancerBo‐Syong Pan0Cheng‐Yu Lin1Gilbert Aaron Lee2Hui‐Kuan Lin3Department of Pathology Duke University Medical Center Durham North Carolina USADepartment of Pathology Duke University Medical Center Durham North Carolina USADepartment of Pathology Duke University Medical Center Durham North Carolina USADepartment of Pathology Duke University Medical Center Durham North Carolina USAAbstract SET domain bifurcated histone lysine methyltransferase 1 (SETDB1/ESET), a pivotal H3K9 methyltransferase, has been extensively studied since its discovery over two decades ago. SETDB1 plays critical roles in immune regulation, including B cell maturation, T‐cell activity modulation, and endogenous retrovirus (ERV) silencing. While essential for normal immune cell function, SETDB1 overexpression in cancer cells disrupts immune responses by suppressing tumor immunogenicity and facilitating immune evasion. This is achieved through the repression of anti‐tumor immune cell production, ERV silencing, and interference with the type I interferon pathway leading to inhibiting immune checkpoint blockade (ICB) efficacy. Beyond its immunological implications, SETDB1 overexpression fosters tumor growth and metastasis via transcriptional silencing of tumor suppressor genes through histone regulation and activating oncogenic signaling by non‐histone regulation. These multifaceted roles make SETDB1 an attractive epigenetic target for novel cancer therapies. This review explores SETDB1's dual function in immune regulation and tumor progression, emphasizing its potential in the development of innovative cancer treatments targeting epigenetic dysregulation and oncogenic signaling.https://doi.org/10.1002/kjm2.12933cancerendogenous retrovirus silencingimmune checkpoint blockagemethyltransferaseSETDB1
spellingShingle Bo‐Syong Pan
Cheng‐Yu Lin
Gilbert Aaron Lee
Hui‐Kuan Lin
Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer
Kaohsiung Journal of Medical Sciences
cancer
endogenous retrovirus silencing
immune checkpoint blockage
methyltransferase
SETDB1
title Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer
title_full Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer
title_fullStr Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer
title_full_unstemmed Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer
title_short Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer
title_sort targeting setdb1 in cancer and immune regulation potential therapeutic strategies in cancer
topic cancer
endogenous retrovirus silencing
immune checkpoint blockage
methyltransferase
SETDB1
url https://doi.org/10.1002/kjm2.12933
work_keys_str_mv AT bosyongpan targetingsetdb1incancerandimmuneregulationpotentialtherapeuticstrategiesincancer
AT chengyulin targetingsetdb1incancerandimmuneregulationpotentialtherapeuticstrategiesincancer
AT gilbertaaronlee targetingsetdb1incancerandimmuneregulationpotentialtherapeuticstrategiesincancer
AT huikuanlin targetingsetdb1incancerandimmuneregulationpotentialtherapeuticstrategiesincancer