Related Experiment Video

Updated: Nov 21, 2025

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

21.4K

Antineoplastic Activity of an Old Natural Antidiabetic Biguanide on the Human Thyroid Carcinoma Cell Line

Zahra Nozhat1, Maryam Zarkesh1, Enke Baldini2

  • 1Cellular and Molecular Endocrine Research Center, Research Institute of Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Anti-Cancer Agents in Medicinal Chemistry
|January 19, 2021
PubMed
Abstract

Insights

Metformin (Met) reduced Medullary Thyroid Carcinoma (MTC) cell viability but may not be suitable for MTC treatment due to RET proto-oncogene induction and FOXO1 inhibition. Further research is needed for thyroid cancer applications.

Area of Science:

  • Endocrinology
  • Oncology
  • Pharmacology

Background:

  • Metformin (Met), an anti-diabetic drug, has emerged as a potential anti-cancer agent.
  • Thyroid cancers represent the most prevalent endocrine system malignancy.

Purpose of the Study:

  • To investigate the effects of Met on Medullary Thyroid Carcinoma (MTC) cell proliferation.
  • To assess Met's impact on the Phosphoinositide 3-Kinase (PI3K)/Protein kinase B (AKT)/Forkhead Box O1 (FOXO1) signaling pathway.
  • To examine Met's influence on the REarranged during Transfection (RET) proto-oncogene expression in MTC cells.

Main Methods:

  • MTC cell line (TT) exposure to varying Met concentrations (0-60 mM) for 24, 48, and 72 hours.
  • Cell viability assessed via MTT assay; apoptosis evaluated using Annexin V-PI staining.
  • Gene expression analysis (PI3K, AKT, FOXO1, RET) by qRT-PCR; protein phosphorylation determined by ELISA.

Main Results:

  • Met significantly reduced MTC cell viability.
  • Met decreased the expression of PI3K, AKT, and FOXO1 genes (P<0.05).
  • Met increased the expression of the RET proto-oncogene (P<0.05).

Conclusions:

  • Met exhibits a cytostatic effect on TT cells.
  • Anti-tumoral effects of Met appear to be cell type-specific.
  • Met is likely unsuitable for MTC treatment due to RET proto-oncogene induction and FOXO1 tumor suppressor gene inhibition, necessitating further research into its mechanisms in thyroid cancers.
Keywords:
Thyroid cancerbiguanidescell signallingdiabetesmetforminproliferation

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.6K
Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma06:08

Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma

Published on: June 2, 2023

2.0K

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...
451
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
4.3K
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
6.4K
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
414
Oral Hypoglycemic Agents: Sulfonylureas01:17

Oral Hypoglycemic Agents: Sulfonylureas

Sulfonylureas are oral hypoglycemic agents utilized in treating type 2 diabetes. They are characterized by their unique sulfonylurea chemical structure. The family of sulfonylureas is divided into generations. First-generation sulfonylureas, including tolbutamide (Orinase), chlorpropamide (Diabinese), and tolazamide (Tolinase), trigger insulin release from pancreatic β cells and enhance peripheral tissues' insulin sensitivity. The second-generation members, such as glipizide...
531