Cyanidin-3-glucoside Hinders Neoplastic Progression in a Spontaneous Mammary Tumor Model
Jen-Yu Chuang1, Wen-Chien Huang2,3, Shih-Ping Cheng2,3
1Division of Hematology and Oncology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei, Taiwan, R.O.C.
Background/Aim:
Dietary and lifestyle patterns may help reduce the risk of breast cancer, and cyanidin-3-glucoside (C3G) is the most extensively studied anthocyanin found in fruits and vegetables. This study aimed to investigate the effects of C3G administration in a spontaneous model of mammary tumors.
Materials And Methods:
MMTV-PyVT transgenic mice were randomly assigned to receive either C3G treatment or vehicle, as control. C3G was administered prior to the onset of mammary tumors. After the mice were sacrificed, mammary tumors underwent RNA sequencing.
Results:
Mice that received C3G exhibited a significantly smaller tumor burden and a longer tumor-free interval. Histological analysis revealed a delayed transformation from hyperplasia to invasive carcinoma, which was further confirmed by whole-mount carmine alum staining. Gene Set Enrichment Analysis indicated negative enrichment of the Akt pathway in the C3G group, consistent with the reduced expression of phosphorylated Akt in mammary tumors.
Conclusion:
Administering C3G before the onset of mammary tumors hinders, but does not prevent, the development of hyperplasia and its progression to aggressive carcinomas.
Insights
Cyanidin-3-glucoside (C3G) supplementation before tumor onset reduced mammary tumor burden in mice. While C3G delayed hyperplasia progression, it did not fully prevent invasive carcinoma development.
Area of Science:
- Oncology
- Nutritional Science
- Molecular Biology
Background:
- Dietary patterns and lifestyle choices influence breast cancer risk.
- Cyanidin-3-glucoside (C3G), a prominent anthocyanin in fruits and vegetables, is investigated for its potential chemopreventive properties.
Purpose of the Study:
- To evaluate the efficacy of cyanidin-3-glucoside (C3G) in mitigating mammary tumor development in a spontaneous mouse model.
- To investigate the molecular mechanisms underlying C3G's effects on tumor progression.
Main Methods:
- MMTV-PyVT transgenic mice received C3G or vehicle control prior to tumor onset.
- Mammary tumors were analyzed using RNA sequencing and histological assessments.
- Gene Set Enrichment Analysis (GSEA) was employed to identify affected signaling pathways.
Main Results:
- C3G administration significantly reduced overall tumor burden and extended the tumor-free interval.
- Histological analysis demonstrated a delay in the transition from hyperplasia to invasive carcinoma.
- Gene expression analysis revealed negative enrichment of the Akt pathway, correlating with reduced phosphorylated Akt levels.
Conclusions:
- Preemptive administration of C3G partially inhibits mammary tumor development and progression.
- C3G treatment delays, but does not completely block, the transition to aggressive carcinomas.
- The Akt signaling pathway may be a key mediator of C3G's anti-tumor effects.
