Evidence map›Paper›PMID 42687390›Full record

ArticleCancer medicine2026

QRICH1 Suppresses Glioma Progression by Inducing ER Stress and Activating the PERK-ATF4-CHOP Pathway.

Yunjiang Wang, Min Xu, Zhenglou Chen, Xuqi Huo, Ya Xue, Xiang Ji, Yang Shen, Hongsheng Wang

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Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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8 authors.

Yunjiang WangDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.ORCID https://orcid.org/0009-0004-3052-2261
Min XuDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.
Zhenglou ChenDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.
Xuqi HuoDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.
Ya XueDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.
Xiang JiDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.
Yang ShenDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.
Hongsheng WangDepartment of Neurosurgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu Province, China.

Funding

National Natural Science Foundation of China 82002643
6 · The paper itself

Abstract

backgroundER stress (ERS) influences tumor behavior through the unfolded protein response (UPR), yet its role in glioma is not fully defined. This study investigated the function of the ERS-related regulator QRICH1 in glioma progression.

methodsPublic databases (TCGA and GTEx) were used to evaluate QRICH1 expression, survival, and prognostic significance in glioma. Lentiviral QRICH1 overexpression or knockdown was established in U87 and U251 cells, followed by functional and mechanistic assays. A subcutaneous xenograft model, histological analyses, and immunohistochemistry were performed to validate the biological function of QRICH1 in vivo.

resultsQRICH1 was markedly upregulated in glioma and associated with better patient survival. QRICH1 overexpression suppressed glioma proliferation, migration, and invasion while promoting apoptosis, whereas silencing QRICH1 enhanced malignancy. Mechanistically, QRICH1 activated the PERK-ATF4-CHOP pathway, increased caspase-12 cleavage, and strengthened ERS-induced apoptosis. In vivo, QRICH1 overexpression reduced tumor size and increased apoptotic markers.

conclusionQRICH1 shifts QRICH1 shifts the UPR toward its pro-apoptotic branch, thereby inhibiting glioma progression, and represents a promising prognostic biomarker and therapeutic target.

Indexed as

Activating Transcription Factor 4Brain NeoplasmseIF-2 KinaseEndoplasmic Reticulum StressGliomaTranscription Factor CHOPAnimalsApoptosisCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceActivating Transcription Factor 4ATF4 protein, humanDDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseTranscription Factor CHOPbioinformaticsendoplasmic reticulum stressQRICH1unfolded protein‐response

Identifiers

PMID42687390
PMCPMC13539068

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