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

ABSTRACT:

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 can

SUBMITTER: Mo HY 

PROVIDER: S-EPMC11086033 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature