IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC

Abstract Background Most small cell lung cancer (SCLC) patients exhibit resistance to immune checkpoint inhibitors (ICIs) and demonstrate downregulation of major histocompatibility complex class I (MHC-I) molecules. This study aimed to elucidate the regulatory mechanisms underlying MHC-I expression...

Full description

Saved in:
Bibliographic Details
Main Authors: Yanan Cui, Tianyu Qiu, Jiale Wang, Xinyu Liu, Libo Luo, Jizhong Yin, Xinxin Zhi, Wanying Wang, Gaohua Feng, Chunyan Wu, Zhikai Zhao, Hua Zhang, Fei Li, Fengying Wu, Shengxiang Ren
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Molecular Cancer
Subjects:
Online Access:https://doi.org/10.1186/s12943-025-02383-x
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849403165361831936
author Yanan Cui
Tianyu Qiu
Jiale Wang
Xinyu Liu
Libo Luo
Jizhong Yin
Xinxin Zhi
Wanying Wang
Gaohua Feng
Chunyan Wu
Zhikai Zhao
Hua Zhang
Fei Li
Fengying Wu
Shengxiang Ren
author_facet Yanan Cui
Tianyu Qiu
Jiale Wang
Xinyu Liu
Libo Luo
Jizhong Yin
Xinxin Zhi
Wanying Wang
Gaohua Feng
Chunyan Wu
Zhikai Zhao
Hua Zhang
Fei Li
Fengying Wu
Shengxiang Ren
author_sort Yanan Cui
collection DOAJ
description Abstract Background Most small cell lung cancer (SCLC) patients exhibit resistance to immune checkpoint inhibitors (ICIs) and demonstrate downregulation of major histocompatibility complex class I (MHC-I) molecules. This study aimed to elucidate the regulatory mechanisms underlying MHC-I expression and potential combination strategies. Methods Single-cell and bulk RNA sequencing data from SCLC patients were analyzed. Clinical data from SCLC patients treated with PD-1/PD-L1 inhibitors were used to investigate the associations between treatment efficacy and IFITM3 expression. In vitro and in vivo functional studies were conducted to evaluate the role and mechanisms of IFITM3 in modulating tumor sensitivity to PD-1 inhibitors. Results Integrative analysis of multiple real-world SCLC cohorts confirmed a significant positive association between IFITM3 expression and MHCI. IFITM3 overexpression upregulated MHC-I-related genes, enriched antigen presentation pathways, and increased CD8+ T-cell infiltration and cytotoxicity. Elevated IFITM3 expression was significantly associated with prolonged progression-free survival (PFS) in patients receiving chemoimmunotherapy but not in those treated with chemotherapy alone. Additionally, patients with high H-scores for IFITM3, as determined by immunohistochemistry, demonstrated better clinical outcomes with chemoimmunotherapy. Inducing IFITM3 expression directly or through treatment with ethyl gallate (EG), an IFITM3 inducer, effectively sensitized tumors to PD-1 blockade in SCLC mouse models. Mechanistic studies revealed that IFITM3 upregulates NLRC5, a key transcriptional activator of MHC-I, facilitating its nuclear translocation and thereby increasing MHC-I levels. Conclusions IFITM3 is associated with MHC-I expression and can predict the efficacy of anti-PD-1/-L1 therapy in SCLC patients. IFITM3 inducers potently improved the efficacy of anti-PD1 monotherapy in SCLC.
format Article
id doaj-art-bc1cf4b0119a4c9ea993e76af09d3514
institution Kabale University
issn 1476-4598
language English
publishDate 2025-07-01
publisher BMC
record_format Article
series Molecular Cancer
spelling doaj-art-bc1cf4b0119a4c9ea993e76af09d35142025-08-20T03:37:20ZengBMCMolecular Cancer1476-45982025-07-0124112010.1186/s12943-025-02383-xIFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLCYanan Cui0Tianyu Qiu1Jiale Wang2Xinyu Liu3Libo Luo4Jizhong Yin5Xinxin Zhi6Wanying Wang7Gaohua Feng8Chunyan Wu9Zhikai Zhao10Hua Zhang11Fei Li12Fengying Wu13Shengxiang Ren14Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Pulmonary and Critical Care Medicine, Zhangjiagang Hospital of Traditional Chinese MedicineDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University School of MedicineHillman Cancer Center, UPMCDepartment of Pathology, Frontier Innovation Center, School of Basic Medical Sciences, Fudan UniversityDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of MedicineAbstract Background Most small cell lung cancer (SCLC) patients exhibit resistance to immune checkpoint inhibitors (ICIs) and demonstrate downregulation of major histocompatibility complex class I (MHC-I) molecules. This study aimed to elucidate the regulatory mechanisms underlying MHC-I expression and potential combination strategies. Methods Single-cell and bulk RNA sequencing data from SCLC patients were analyzed. Clinical data from SCLC patients treated with PD-1/PD-L1 inhibitors were used to investigate the associations between treatment efficacy and IFITM3 expression. In vitro and in vivo functional studies were conducted to evaluate the role and mechanisms of IFITM3 in modulating tumor sensitivity to PD-1 inhibitors. Results Integrative analysis of multiple real-world SCLC cohorts confirmed a significant positive association between IFITM3 expression and MHCI. IFITM3 overexpression upregulated MHC-I-related genes, enriched antigen presentation pathways, and increased CD8+ T-cell infiltration and cytotoxicity. Elevated IFITM3 expression was significantly associated with prolonged progression-free survival (PFS) in patients receiving chemoimmunotherapy but not in those treated with chemotherapy alone. Additionally, patients with high H-scores for IFITM3, as determined by immunohistochemistry, demonstrated better clinical outcomes with chemoimmunotherapy. Inducing IFITM3 expression directly or through treatment with ethyl gallate (EG), an IFITM3 inducer, effectively sensitized tumors to PD-1 blockade in SCLC mouse models. Mechanistic studies revealed that IFITM3 upregulates NLRC5, a key transcriptional activator of MHC-I, facilitating its nuclear translocation and thereby increasing MHC-I levels. Conclusions IFITM3 is associated with MHC-I expression and can predict the efficacy of anti-PD-1/-L1 therapy in SCLC patients. IFITM3 inducers potently improved the efficacy of anti-PD1 monotherapy in SCLC.https://doi.org/10.1186/s12943-025-02383-xSmall cell lung cancerImmunotherapyMHC-IIFITM3
spellingShingle Yanan Cui
Tianyu Qiu
Jiale Wang
Xinyu Liu
Libo Luo
Jizhong Yin
Xinxin Zhi
Wanying Wang
Gaohua Feng
Chunyan Wu
Zhikai Zhao
Hua Zhang
Fei Li
Fengying Wu
Shengxiang Ren
IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC
Molecular Cancer
Small cell lung cancer
Immunotherapy
MHC-I
IFITM3
title IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC
title_full IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC
title_fullStr IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC
title_full_unstemmed IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC
title_short IFITM3 enhances immunosensitivity via MHC-I regulation and is associated with the efficacy of anti-PD-1/-L1 therapy in SCLC
title_sort ifitm3 enhances immunosensitivity via mhc i regulation and is associated with the efficacy of anti pd 1 l1 therapy in sclc
topic Small cell lung cancer
Immunotherapy
MHC-I
IFITM3
url https://doi.org/10.1186/s12943-025-02383-x
work_keys_str_mv AT yanancui ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT tianyuqiu ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT jialewang ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT xinyuliu ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT liboluo ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT jizhongyin ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT xinxinzhi ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT wanyingwang ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT gaohuafeng ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT chunyanwu ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT zhikaizhao ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT huazhang ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT feili ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT fengyingwu ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc
AT shengxiangren ifitm3enhancesimmunosensitivityviamhciregulationandisassociatedwiththeefficacyofantipd1l1therapyinsclc