GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT

Abstract Cisplatin (CDDP) based chemotherapy has emerged as the predominant therapeutic regimen for patients with advanced gastric cancer (GC). However, its efficacy is dampened by the development of chemoresistance, which results in poor prognosis of patients. GLI2, a key transcription factor in th...

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Main Authors: Wenshuai Zhu, Jingguo Sun, Fubo Jing, Yuanxin Xing, Muhua Luan, Zhaotian Feng, Xiaoli Ma, Yunshan Wang, Yanfei Jia
Format: Article
Language:English
Published: Nature Publishing Group 2025-03-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-025-07564-6
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author Wenshuai Zhu
Jingguo Sun
Fubo Jing
Yuanxin Xing
Muhua Luan
Zhaotian Feng
Xiaoli Ma
Yunshan Wang
Yanfei Jia
author_facet Wenshuai Zhu
Jingguo Sun
Fubo Jing
Yuanxin Xing
Muhua Luan
Zhaotian Feng
Xiaoli Ma
Yunshan Wang
Yanfei Jia
author_sort Wenshuai Zhu
collection DOAJ
description Abstract Cisplatin (CDDP) based chemotherapy has emerged as the predominant therapeutic regimen for patients with advanced gastric cancer (GC). However, its efficacy is dampened by the development of chemoresistance, which results in poor prognosis of patients. GLI2, a key transcription factor in the Hedgehog (Hh) signaling pathway, is regarded as a target for cancer therapy. However, the significance of GLI2 for CDDP resistance in GC has not been well established. Here, we show that GLI2 expression was upregulated in EMT-type GC and associated with poor prognosis. GLI2 promotes proliferation, migration, and CDDP resistance of GC cells by inducing EMT. In terms of mechanism, GLI2 binds to the promoter region of DEC1 and enhances its expression, thereby co-transcriptionally regulating ZEB1 expression. Animal experiments have demonstrated that both GLI2 knockdown and GLI2 inhibitor significantly enhance CDDP sensitivity in GC. Our data not only identify a novel GLI2/DEC1/ZEB1/EMT pathway in GC CDDP resistance but also provide novel strategies to treat GC in the future.
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id doaj-art-9b3260992e6746c29887a780fa784ba2
institution DOAJ
issn 2041-4889
language English
publishDate 2025-03-01
publisher Nature Publishing Group
record_format Article
series Cell Death and Disease
spelling doaj-art-9b3260992e6746c29887a780fa784ba22025-08-20T02:48:57ZengNature Publishing GroupCell Death and Disease2041-48892025-03-0116111510.1038/s41419-025-07564-6GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMTWenshuai Zhu0Jingguo Sun1Fubo Jing2Yuanxin Xing3Muhua Luan4Zhaotian Feng5Xiaoli Ma6Yunshan Wang7Yanfei Jia8Research Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical UniversityResearch Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical UniversityResearch Center of Basic Medicine, Jinan Central Hospital, Shandong UniversityResearch Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical UniversityResearch Center of Basic Medicine, Jinan Central Hospital, Shandong UniversityDepartment of Medical Laboratory, Shandong Second Medical UniversityResearch Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical UniversityResearch Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical UniversityResearch Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical UniversityAbstract Cisplatin (CDDP) based chemotherapy has emerged as the predominant therapeutic regimen for patients with advanced gastric cancer (GC). However, its efficacy is dampened by the development of chemoresistance, which results in poor prognosis of patients. GLI2, a key transcription factor in the Hedgehog (Hh) signaling pathway, is regarded as a target for cancer therapy. However, the significance of GLI2 for CDDP resistance in GC has not been well established. Here, we show that GLI2 expression was upregulated in EMT-type GC and associated with poor prognosis. GLI2 promotes proliferation, migration, and CDDP resistance of GC cells by inducing EMT. In terms of mechanism, GLI2 binds to the promoter region of DEC1 and enhances its expression, thereby co-transcriptionally regulating ZEB1 expression. Animal experiments have demonstrated that both GLI2 knockdown and GLI2 inhibitor significantly enhance CDDP sensitivity in GC. Our data not only identify a novel GLI2/DEC1/ZEB1/EMT pathway in GC CDDP resistance but also provide novel strategies to treat GC in the future.https://doi.org/10.1038/s41419-025-07564-6
spellingShingle Wenshuai Zhu
Jingguo Sun
Fubo Jing
Yuanxin Xing
Muhua Luan
Zhaotian Feng
Xiaoli Ma
Yunshan Wang
Yanfei Jia
GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT
Cell Death and Disease
title GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT
title_full GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT
title_fullStr GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT
title_full_unstemmed GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT
title_short GLI2 inhibits cisplatin sensitivity in gastric cancer through DEC1/ZEB1 mediated EMT
title_sort gli2 inhibits cisplatin sensitivity in gastric cancer through dec1 zeb1 mediated emt
url https://doi.org/10.1038/s41419-025-07564-6
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