Naringenin suppresses epithelial ovarian cancer by inhibiting proliferation and modulating gut microbiota
Related Experiment Video
Updated: Aug 30, 2025
Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Caiji Lin1, Zheng Zeng1, Yiru Lin1
1Genomics Research Center (State-Province Key Laboratory of Biomedicine-Pharmaceutics of China), College of Pharmacy, Harbin Medical University, Harbin 150081, China; Harbin Medical University-University of Calgary Cumming School of Medicine Centre for Infection and Genomics, Harbin Medical University, Harbin 150081, China; Translational Medicine Research and Cooperation Center of Northern China, Heilongjiang Academy of Medical Sciences, Harbin 150081, China.
Background:
Ovarian cancer has the highest mortality among all gynecological malignancies; currently, no effective therapeutics are available for its treatment. Naringenin has been shown to inhibit the progression of various cancers, but its inhibitory effect on ovarian cancer remains unknown.
Purpose:
This study aimed to evaluate the inhibitory effects of naringenin on ovarian cancer and elucidate the underlying mechanisms.
Methods:
Cancer cell proliferation was detected by cell counting kit-8 and crystal violet assays, and the migration capability was determined by wound healing and transwell assays. Western blotting and immunohistochemistry assays were employed to determine the expression levels of the epidermal growth factor receptor, phosphatidylinositol 3-kinase (PI3K) and cyclin D1 in vitro and in vivo, respectively. An ES-2 xenograft nude mouse model was established for the in vivo experiments, and fecal samples were collected for intestinal microbiota analysis by 16S rDNA sequencing.
Results:
Naringenin suppressed the proliferation and migration of A2780 and ES-2 cancer cell lines and downregulated PI3K in vitro. In animal experiments, naringenin treatment significantly decreased the tumor weight and volume, and oral administration exhibited greater effects than intraperitoneal injection. Additionally, naringenin treatment ameliorated the population composition of the microbiota in animals with ovarian cancer and significantly increased the abundances of Alistipes and Lactobacillus.
Conclusion:
Naringenin suppresses epithelial ovarian cancer by inhibiting PI3K pathway expression and ameliorating the gut microbiota, and the oral route is more effective than parenteral administration.
Insights
Naringenin inhibits ovarian cancer progression by reducing cell proliferation and migration. Oral naringenin administration is more effective, also improving gut microbiota composition.
Area of Science:
- Oncology
- Pharmacology
- Microbiome Research
Background:
- Ovarian cancer presents a high mortality rate with limited therapeutic options.
- Naringenin demonstrates anti-cancer properties, but its effect on ovarian cancer is unexplored.
Purpose of the Study:
- To investigate the inhibitory effects of naringenin on ovarian cancer.
- To elucidate the molecular mechanisms underlying naringenin's action.
Main Methods:
- Cell proliferation and migration assays (CCK-8, crystal violet, wound healing, transwell).
- Western blotting and immunohistochemistry for PI3K, EGFR, and cyclin D1.
- In vivo ES-2 xenograft model and 16S rDNA sequencing for gut microbiota analysis.
Main Results:
- Naringenin suppressed ovarian cancer cell proliferation and migration, downregulating PI3K.
- Oral naringenin significantly reduced tumor weight and volume in vivo.
- Naringenin altered gut microbiota composition, increasing beneficial bacteria like Alistipes and Lactobacillus.
Conclusions:
- Naringenin inhibits epithelial ovarian cancer via PI3K pathway suppression and gut microbiota modulation.
- Oral administration of naringenin is more effective than parenteral routes.
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