Related Experiment Video

Updated: May 7, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.1K

Metallothionein 1G functions as a tumor suppressor in thyroid cancer through modulating the PI3K/Akt signaling

Jiao Fu1, Hongjun Lv, Haixia Guan

  • 1Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University School of Medicine, Xi'an 710061, China. phou@mail.xjtu.edu.cn.

BMC Cancer
|October 9, 2013
PubMed
Abstract

Insights

Metallothionein-1G (MT1G) acts as a tumor suppressor in thyroid cancer by inhibiting cell growth and metastasis. Its inactivation through promoter methylation is linked to papillary thyroid cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Metallothionein-1G (MT1G) inactivation via promoter methylation is observed in thyroid cancer.
  • The precise role of MT1G in thyroid carcinogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the biological functions of MT1G in thyroid cancer.
  • To explore the molecular mechanisms underlying MT1G's role in thyroid tumorigenesis.

Main Methods:

  • Analyzed MT1G promoter methylation and its correlation with clinicopathological features in papillary thyroid cancer (PTC) using methylation-specific PCR (MSP).
  • Assessed MT1G mRNA expression via RT-PCR.
  • Evaluated the functional impact of MT1G restoration on cell proliferation, cell cycle, apoptosis, migration, and invasion.

Main Results:

  • MT1G expression is frequently silenced or downregulated in thyroid cancer cell lines and tissues.
  • MT1G inactivation is attributed to promoter methylation and histone modification.
  • MT1G hypermethylation positively correlates with lymph node metastasis in PTC.
  • Restoring MT1G expression inhibits cell growth, invasiveness, and induces cell cycle arrest and apoptosis by inhibiting Akt and Rb phosphorylation.

Conclusions:

  • MT1G functions as a tumor suppressor in thyroid carcinogenesis.
  • MT1G modulates the phosphatidylinositol-3-kinase (PI3K)/Akt and Rb/E2F pathways.
  • MT1G inactivation is a significant event in thyroid cancer development.

More Related Videos

Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies07:47

Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies

Published on: September 15, 2023

2.2K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.3K

Related Concept Videos

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...
3.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.2K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.3K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

2.7K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K