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Updated: Feb 4, 2026

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
Published on: May 17, 2018
Compound Fuling Granule Suppresses Ovarian Cancer Development and Progression by disrupting mitochondrial function,
Shanming Ruan1, Zhiqian Zhang2,3, Xinxin Tian2,4
1Department of Medical Oncology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310003, Zhejiang, China.
Abstract:
Our previous studies have demonstrated that the compound fuling granule (CFG), a traditional Chinese medicine, suppresses ovarian cancer cell growth, migration and metastasis. However, the underlying mechanisms remain to be fully elucidated. In this study, we found that CFG could induce mitochondrial fragmentation, mitochondrial membrane potential reduction and cytochrome c release in ovarian SKOV3 cancer cells. In addition, both metabolomics and transcriptomics approaches were applied to illustrate the systemic mechanism of CFG on ovarian cancer formation and progression. To this end, we established two tumor-bearing mice models with subcutaneous injection or tail intravenous injection. Functionally, administration of CFG suppresses in situ tumor growth and distant lung metastasis. Subsequently, gas chromatography-mass spectrometry (GC-MS) was applied to determine the metabolic alterations among the plasma samples from these in vivo models. In the subcutaneous injection model, 26 distinguishable metabolites were identified and 12 metabolic pathways were reprogrammed. Meanwhile, 19 metabolites involved in 7 metabolic pathways showed significant differences in the tail intravenous injection model. Importantly, integrative metabolomics and transcriptomics analysis showed these metabolites were highly associated with galactose metabolism and fatty acid metabolism. This study suggests that CFG may suppress ovarian cancer cell proliferation and metastasis by regulating mitochondrion-related energy metabolisms.
Insights
Compound Fuling Granule (CFG) suppresses ovarian cancer progression by disrupting mitochondrial function and altering key metabolic pathways like galactose and fatty acid metabolism. This traditional Chinese medicine shows promise in inhibiting tumor growth and metastasis.
Area of Science:
- Oncology
- Pharmacology
- Metabolomics
Background:
- Compound Fuling Granule (CFG), a traditional Chinese medicine, has shown potential in suppressing ovarian cancer.
- The precise mechanisms by which CFG exerts its anti-cancer effects require further elucidation.
Purpose of the Study:
- To investigate the underlying mechanisms of CFG in inhibiting ovarian cancer cell growth, migration, and metastasis.
- To explore the systemic effects of CFG on ovarian cancer progression using metabolomics and transcriptomics.
Main Methods:
- Ovarian SKOV3 cancer cells were treated with CFG to assess mitochondrial function (fragmentation, membrane potential, cytochrome c release).
- Two in vivo mouse models (subcutaneous and tail intravenous injection) were established to evaluate CFG's effect on tumor growth and metastasis.
- Gas chromatography-mass spectrometry (GC-MS) was used for metabolomic profiling of plasma samples.
- Integrative analysis of metabolomics and transcriptomics data was performed.
Main Results:
- CFG induced mitochondrial fragmentation, reduced mitochondrial membrane potential, and promoted cytochrome c release in ovarian cancer cells.
- In vivo administration of CFG suppressed both in situ tumor growth and lung metastasis.
- Metabolomic analysis identified significant alterations in 26 metabolites (12 pathways) in the subcutaneous model and 19 metabolites (7 pathways) in the intravenous model.
- Integrative analysis linked these metabolic changes to galactose and fatty acid metabolism.
Conclusions:
- CFG suppresses ovarian cancer progression by impacting mitochondrial function and energy metabolism.
- CFG may exert its anti-cancer effects through the regulation of galactose and fatty acid metabolic pathways.
- These findings highlight CFG as a potential therapeutic agent for ovarian cancer, warranting further investigation into its mitochondrion-related metabolic regulatory mechanisms.
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