KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells

Abstract Cancer stem cells (CSCs) play crucial roles in tumor metastasis, therapy resistance, and immune evasion. Identifying and understanding the factors that regulate the stemness of tumor cells presents promising opportunities for developing effective therapeutic strategies. In this study on ora...

Full description

Saved in:
Bibliographic Details
Main Authors: Xin Qi, Jiang Zhou, Pan Wang, Yunyan Li, Haoran Li, Yuwen Miao, XiaoQing Ma, Xiayan Luo, Zhiling Zhang, Yanling He, Wenyi Shen, Wenquan Zhao, Rutao Cui, Cang Li, Huiyong Zhu, Jiong Lyu
Format: Article
Language:English
Published: Nature Publishing Group 2025-05-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-025-07689-8
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850206276822237184
author Xin Qi
Jiang Zhou
Pan Wang
Yunyan Li
Haoran Li
Yuwen Miao
XiaoQing Ma
Xiayan Luo
Zhiling Zhang
Yanling He
Wenyi Shen
Wenquan Zhao
Rutao Cui
Cang Li
Huiyong Zhu
Jiong Lyu
author_facet Xin Qi
Jiang Zhou
Pan Wang
Yunyan Li
Haoran Li
Yuwen Miao
XiaoQing Ma
Xiayan Luo
Zhiling Zhang
Yanling He
Wenyi Shen
Wenquan Zhao
Rutao Cui
Cang Li
Huiyong Zhu
Jiong Lyu
author_sort Xin Qi
collection DOAJ
description Abstract Cancer stem cells (CSCs) play crucial roles in tumor metastasis, therapy resistance, and immune evasion. Identifying and understanding the factors that regulate the stemness of tumor cells presents promising opportunities for developing effective therapeutic strategies. In this study on oral squamous cell carcinoma (OSCC), we confirmed the key role of KLF7 in maintaining the stemness of OSCC. Using chromatin immunoprecipitation sequencing and dual-luciferase assays, we identified ITGA2, a membrane receptor, as a key downstream gene regulated by KLF7 in the maintenance of stemness. Tumor sphere formation assays, flow cytometry analyses, and in vivo limiting dilution tumorigenicity evaluations demonstrated that knocking down ITGA2 significantly impaired stemness. Upon binding to its extracellular matrix (ECM) ligand, type I collagen, ITGA2 activates stemness-associated signaling pathways, including PI3K-AKT, MAPK, and Hippo. TC-I 15, a small-molecule inhibitor of the ITGA2-collagen interaction, significantly sensitizes oral squamous cell carcinoma (OSCC) to cisplatin in xenograft models. In summary, we reveal that the KLF7/ITGA2 axis is a crucial modulator of stemness in OSCC. Our findings suggest that ITGA2 is a promising therapeutic target, offering a novel anti-CSC strategy.
format Article
id doaj-art-2a5a9d1b9bb04bb88f37c7624fcf9a5f
institution OA Journals
issn 2041-4889
language English
publishDate 2025-05-01
publisher Nature Publishing Group
record_format Article
series Cell Death and Disease
spelling doaj-art-2a5a9d1b9bb04bb88f37c7624fcf9a5f2025-08-20T02:10:53ZengNature Publishing GroupCell Death and Disease2041-48892025-05-0116111310.1038/s41419-025-07689-8KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cellsXin Qi0Jiang Zhou1Pan Wang2Yunyan Li3Haoran Li4Yuwen Miao5XiaoQing Ma6Xiayan Luo7Zhiling Zhang8Yanling He9Wenyi Shen10Wenquan Zhao11Rutao Cui12Cang Li13Huiyong Zhu14Jiong Lyu15Zhejiang University, School of Medicine, First Affiliated HospitalCancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of MedicineDepartment of Stomatology, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child HealthCancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of MedicineZhejiang University, School of Medicine, First Affiliated HospitalZhejiang University, School of Medicine, Affiliated Stomatology HospitalCancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of MedicineZhejiang University, School of Medicine, First Affiliated HospitalCancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of MedicineZhejiang University, School of Medicine, First Affiliated HospitalZhejiang University, School of Medicine, First Affiliated HospitalZhejiang University, School of Medicine, First Affiliated HospitalCancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of MedicineCancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of MedicineZhejiang University, School of Medicine, First Affiliated HospitalZhejiang University, School of Medicine, First Affiliated HospitalAbstract Cancer stem cells (CSCs) play crucial roles in tumor metastasis, therapy resistance, and immune evasion. Identifying and understanding the factors that regulate the stemness of tumor cells presents promising opportunities for developing effective therapeutic strategies. In this study on oral squamous cell carcinoma (OSCC), we confirmed the key role of KLF7 in maintaining the stemness of OSCC. Using chromatin immunoprecipitation sequencing and dual-luciferase assays, we identified ITGA2, a membrane receptor, as a key downstream gene regulated by KLF7 in the maintenance of stemness. Tumor sphere formation assays, flow cytometry analyses, and in vivo limiting dilution tumorigenicity evaluations demonstrated that knocking down ITGA2 significantly impaired stemness. Upon binding to its extracellular matrix (ECM) ligand, type I collagen, ITGA2 activates stemness-associated signaling pathways, including PI3K-AKT, MAPK, and Hippo. TC-I 15, a small-molecule inhibitor of the ITGA2-collagen interaction, significantly sensitizes oral squamous cell carcinoma (OSCC) to cisplatin in xenograft models. In summary, we reveal that the KLF7/ITGA2 axis is a crucial modulator of stemness in OSCC. Our findings suggest that ITGA2 is a promising therapeutic target, offering a novel anti-CSC strategy.https://doi.org/10.1038/s41419-025-07689-8
spellingShingle Xin Qi
Jiang Zhou
Pan Wang
Yunyan Li
Haoran Li
Yuwen Miao
XiaoQing Ma
Xiayan Luo
Zhiling Zhang
Yanling He
Wenyi Shen
Wenquan Zhao
Rutao Cui
Cang Li
Huiyong Zhu
Jiong Lyu
KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells
Cell Death and Disease
title KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells
title_full KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells
title_fullStr KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells
title_full_unstemmed KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells
title_short KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells
title_sort klf7 regulated itga2 as a therapeutic target for inhibiting oral cancer stem cells
url https://doi.org/10.1038/s41419-025-07689-8
work_keys_str_mv AT xinqi klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT jiangzhou klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT panwang klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT yunyanli klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT haoranli klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT yuwenmiao klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT xiaoqingma klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT xiayanluo klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT zhilingzhang klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT yanlinghe klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT wenyishen klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT wenquanzhao klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT rutaocui klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT cangli klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT huiyongzhu klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells
AT jionglyu klf7regulateditga2asatherapeutictargetforinhibitingoralcancerstemcells