Related Experiment Video
Updated: Oct 29, 2025
Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
Published on: June 20, 2015
Metformin Antagonizes Ovarian Cancer Cells Malignancy Through MSLN Mediated IL-6/STAT3 Signaling
Xu Yang1, Mei Huang1, Qin Zhang1
1Department of Obstetrics and Gynecology, The Fifth Affiliated People's Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, People's Republic of China.
Background:
Ovarian cancer is the most lethal gynecological malignancy, and chemotherapy remains the cornerstone for ovarian cancer management. Due to the unsatisfactory prognosis, a better understanding of the underlying molecular carcinogenesis is urgently required.
Methods:
Assays for determining cell growth, cell motility, and apoptosis were employed to evaluate the potential antitumor effects of metformin against ovarian cancer cells. Molecular biological methods were employed to explore the underlying mechanism. Human ovarian cancer samples and Gene Expression Profiling Interactive Analysis (GEPIA) dataset were used for uncovering the clinical significances of mesothelin (MSLN) on ovarian cancer.
Results:
In the present work, we found that metformin treatment led to cell growth and cell migration inhibition, and induced cell apoptosis. Metformin administration also impaired cancer cell stemness and the capillary-like structure formation capacity of SKOV3 cells. On mechanism, metformin treatment remarkably reduced mesothelin (MSLN) expression, downregulated IL-6/STAT3 signaling activity, subsequently resulted in VEGF and TGFβ1 expression. We also observed an oncogenic function of MSLN on ovarian cancer.
Conclusions:
Collectively, our findings suggested that metformin exerts anticancer effects by suppressing ovarian cancer cell malignancy, which attributed to MSLN inhibition mediated IL6/STAT3 signaling and VEGF and TGFβ1 downregulation.
Insights
Metformin inhibits ovarian cancer growth, migration, and stemness by reducing mesothelin (MSLN) expression. This action downregulates IL-6/STAT3 signaling, decreasing VEGF and TGFβ1, crucial for cancer progression.
Area of Science:
- Gynecologic Oncology
- Molecular Carcinogenesis
- Pharmacology
Background:
- Ovarian cancer is a leading cause of gynecological cancer mortality.
- Chemotherapy is the primary treatment, but prognosis remains poor.
- Understanding molecular drivers is crucial for improved ovarian cancer therapies.
Purpose of the Study:
- To evaluate the antitumor effects of metformin on ovarian cancer cells.
- To elucidate the underlying molecular mechanisms of metformin's action.
- To investigate the clinical significance of mesothelin (MSLN) in ovarian cancer.
Main Methods:
- Cell growth, motility, and apoptosis assays were performed.
- Molecular biology techniques explored metformin's mechanism of action.
- Human ovarian cancer samples and GEPIA dataset analyzed MSLN significance.
Main Results:
- Metformin inhibited ovarian cancer cell growth, migration, and stemness.
- Metformin induced apoptosis and impaired capillary-like structure formation.
- Metformin reduced mesothelin (MSLN) expression, downregulating IL-6/STAT3, VEGF, and TGFβ1.
Conclusions:
- Metformin exhibits anticancer effects in ovarian cancer by suppressing malignancy.
- Metformin's efficacy is linked to MSLN inhibition and downstream signaling pathways.
- MSLN plays an oncogenic role in ovarian cancer progression.
Related Concept Videos
01:26Oral Hypoglycemic Agents: Biguanides and Glitazones
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
02:23Abnormal Proliferation