Related Experiment Video

Updated: May 20, 2026

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

Metformin inhibits the development and metastasis of ovarian cancer

Buchu Wu1, Shu Li, Lili Sheng

  • 1Department of Obstetrics and Gynecology, Ren-Ji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.

Oncology Reports
|July 4, 2012
PubMed

Insights

Metformin significantly inhibits ovarian cancer cell development and metastasis in vitro and in vivo. It reduces cell adhesion, invasion, and migration, while also decreasing angiogenesis and macrophage infiltration.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Ovarian cancer is a leading cause of cancer-related deaths in women.
  • Metformin, a common diabetes drug, has shown potential anti-cancer properties.
  • Understanding metformin's mechanism in ovarian cancer is crucial for therapeutic development.

Purpose of the Study:

  • To investigate metformin's role in regulating ovarian cancer cell development and metastasis.
  • To assess metformin's effects on ovarian cancer cell adhesion, invasion, and migration in vitro.
  • To evaluate metformin's impact on tumor growth, metastasis, angiogenesis, and macrophage infiltration in vivo.

Main Methods:

  • In vitro studies utilized cell adhesion, invasion, and migration tests on ovarian cancer cell lines (SKOV3, HO8910-PM).
  • In vivo studies involved administering intraperitoneal metformin to nude mice bearing ovarian tumors.
  • Tumor size, metastatic tumor count, angiogenesis (vWF), and macrophage infiltration were quantified.

Main Results:

  • Metformin demonstrated a dose-dependent inhibition of ovarian cancer cell proliferation, migration, invasion, and adhesion in vitro (P<0.05).
  • In vivo, metformin significantly inhibited hepatic, intestinal, and lung metastasis (P<0.05) without causing weight loss.
  • Decreased expression of von Willebrand Factor (vWF) and reduced macrophage infiltration were observed in tumors.

Conclusions:

  • Metformin effectively inhibits ovarian cancer development and metastasis.
  • The drug's action involves reducing cellular-extracellular matrix interactions, neovascularization, and macrophage infiltration.
  • Metformin presents a promising therapeutic agent for ovarian cancer treatment.

More Related Videos

Quantitation of Intra-peritoneal Ovarian Cancer Metastasis10:58

Quantitation of Intra-peritoneal Ovarian Cancer Metastasis

Published on: July 18, 2016

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum05:42

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum

Published on: January 26, 2024

Related Concept Videos

Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...