MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions

Objectives: Cancer cells undergo metabolic reprogramming to adapt to high oxidative stress, but little is known about how metabolic remodeling enables gastric cancer cells to survive stress associated with aberrant reactive oxygen species (ROS) production. Here, we aimed to identify the key metaboli...

Full description

Saved in:
Bibliographic Details
Main Authors: Hai-Yu Mo, Ruo-Bing Wang, Meng-Yao Ma, Yi Zhang, Xin-Yu Li, Wang-Rong Wen, Yi Han, Tian Tian
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Redox Report
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/13510002.2024.2345455
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850112199113048064
author Hai-Yu Mo
Ruo-Bing Wang
Meng-Yao Ma
Yi Zhang
Xin-Yu Li
Wang-Rong Wen
Yi Han
Tian Tian
author_facet Hai-Yu Mo
Ruo-Bing Wang
Meng-Yao Ma
Yi Zhang
Xin-Yu Li
Wang-Rong Wen
Yi Han
Tian Tian
author_sort Hai-Yu Mo
collection DOAJ
description Objectives: Cancer cells undergo metabolic reprogramming to adapt to high oxidative stress, but little is known about how metabolic remodeling enables gastric cancer cells to survive stress associated with aberrant reactive oxygen species (ROS) production. Here, we aimed to identify the key metabolic enzymes that protect gastric cancer (GC) cells from oxidative stress.Methods: ROS level was detected by DCFH-DA probes. Multiple cell biological studies were performed to identify the underlying mechanisms. Furthermore, cell-based xenograft and patient-derived xenograft (PDX) model were performed to evaluate the role of MTHFD2 in vivo.Results: We found that overexpression of MTHFD2, but not MTHFD1, is associated with reduced overall and disease-free survival in gastric cancer. In addition, MTHFD2 knockdown reduces the cellular NADPH/NADP+ ratio, colony formation and mitochondrial function, increases cellular ROS and cleaved PARP levels and induces in cell death under hypoxia, a hallmark of solid cancers and a common inducer of oxidative stress. Moreover, genetic or pharmacological inhibition of MTHFD2 reduces tumor burden in both tumor cell lines and patient-derived xenograft-based models.Discussion: our study highlights the crucial role of MTHFD2 in redox regulation and tumor progression, demonstrating the therapeutic potential of targeting MTHFD2.
format Article
id doaj-art-885fc61a67754f1fbb20a47ce39e66fa
institution OA Journals
issn 1351-0002
1743-2928
language English
publishDate 2024-12-01
publisher Taylor & Francis Group
record_format Article
series Redox Report
spelling doaj-art-885fc61a67754f1fbb20a47ce39e66fa2025-08-20T02:37:28ZengTaylor & Francis GroupRedox Report1351-00021743-29282024-12-0129110.1080/13510002.2024.2345455MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditionsHai-Yu Mo0Ruo-Bing Wang1Meng-Yao Ma2Yi Zhang3Xin-Yu Li4Wang-Rong Wen5Yi Han6Tian Tian7Department of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People’s Republic of ChinaDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People’s Republic of ChinaDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People’s Republic of ChinaState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, People’s Republic of ChinaDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People’s Republic of ChinaClinical Laboratory, The Affiliated Shunde Hospital of Jinan University, Foshan, People’s Republic of ChinaState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, People’s Republic of ChinaDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People’s Republic of ChinaObjectives: Cancer cells undergo metabolic reprogramming to adapt to high oxidative stress, but little is known about how metabolic remodeling enables gastric cancer cells to survive stress associated with aberrant reactive oxygen species (ROS) production. Here, we aimed to identify the key metabolic enzymes that protect gastric cancer (GC) cells from oxidative stress.Methods: ROS level was detected by DCFH-DA probes. Multiple cell biological studies were performed to identify the underlying mechanisms. Furthermore, cell-based xenograft and patient-derived xenograft (PDX) model were performed to evaluate the role of MTHFD2 in vivo.Results: We found that overexpression of MTHFD2, but not MTHFD1, is associated with reduced overall and disease-free survival in gastric cancer. In addition, MTHFD2 knockdown reduces the cellular NADPH/NADP+ ratio, colony formation and mitochondrial function, increases cellular ROS and cleaved PARP levels and induces in cell death under hypoxia, a hallmark of solid cancers and a common inducer of oxidative stress. Moreover, genetic or pharmacological inhibition of MTHFD2 reduces tumor burden in both tumor cell lines and patient-derived xenograft-based models.Discussion: our study highlights the crucial role of MTHFD2 in redox regulation and tumor progression, demonstrating the therapeutic potential of targeting MTHFD2.https://www.tandfonline.com/doi/10.1080/13510002.2024.2345455Gastric cancermethylene tetrahydrofolate dehydrogenase 2 (MTHFD2)redox metabolismNADPHreactive oxygen species (ROS)
spellingShingle Hai-Yu Mo
Ruo-Bing Wang
Meng-Yao Ma
Yi Zhang
Xin-Yu Li
Wang-Rong Wen
Yi Han
Tian Tian
MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
Redox Report
Gastric cancer
methylene tetrahydrofolate dehydrogenase 2 (MTHFD2)
redox metabolism
NADPH
reactive oxygen species (ROS)
title MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
title_full MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
title_fullStr MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
title_full_unstemmed MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
title_short MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
title_sort mthfd2 mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions
topic Gastric cancer
methylene tetrahydrofolate dehydrogenase 2 (MTHFD2)
redox metabolism
NADPH
reactive oxygen species (ROS)
url https://www.tandfonline.com/doi/10.1080/13510002.2024.2345455
work_keys_str_mv AT haiyumo mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT ruobingwang mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT mengyaoma mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT yizhang mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT xinyuli mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT wangrongwen mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT yihan mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions
AT tiantian mthfd2mediatedredoxhomeostasispromotesgastriccancerprogressionunderhypoxicconditions