Related Experiment Video
Updated: Mar 31, 2026

Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids
Published on: October 21, 2022
CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer
Jiebang Jiang1, Xinxin Zhang1, Yipeng Sun1
1School of Life Sciences, Jiangsu Normal University, Xuzhou, Jiangsu 221116, China.
Abstract:
Colorectal cancer (CRC) remains a leading cause of cancer mortality, necessitating effective therapeutic strategies. This study investigates the antitumor properties and mechanism of Cya-Gly-Fer (CGF), a natural anthocyanin derivative. Using CRC cell lines, organoids, and xenograft models, we show that CGF significantly inhibits tumor growth and metastasis. Integrated transcriptomics and metabolomics indicate that CGF disrupts central carbon metabolism and oxidative phosphorylation. Mechanistically, CGF downregulation of ABC transporters causes intracellular ATP accumulation, triggering mitochondrial dysfunction and excessive reactive oxygen species (ROS) generation. This metabolic stress suppresses the MAPK/ERK1/2/c-MYC signaling axis, leading to cell-cycle arrest and apoptosis. These findings identify CGF as a potent agent that targets mitochondrial homeostasis to halt CRC progression.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Mitogens and the Cell Cycle
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
PI3K/mTOR/AKT Signaling Pathway

