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Related Concept Videos

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 daughter...
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.
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PI3K/mTOR/AKT Signaling Pathway

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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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Cancer-Critical Genes II: Tumor Suppressor Genes

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Related Experiment Video

Updated: May 18, 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

SIRT1 promotes thyroid carcinogenesis driven by PTEN deficiency.

D Herranz1, A Maraver, M Cañamero

  • 1Tumor Suppression Group, Spanish National Cancer Research Center (CNIO), Madrid, Spain.

Oncogene
|September 19, 2012
PubMed
Summary
This summary is machine-generated.

SIRT1, previously thought to suppress tumors, acts as an oncogene in mouse thyroid and prostate cancers by increasing c-MYC. This finding suggests SIRT1 as a potential therapeutic target for thyroid carcinomas.

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Spontaneous Murine Model of Anaplastic Thyroid Cancer
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Spontaneous Murine Model of Anaplastic Thyroid Cancer

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Last Updated: May 18, 2026

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Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • SIRT1 is generally considered a tumor suppressor based on mouse models.
  • Previous research has not identified oncogenic roles for SIRT1 in vivo.

Purpose of the Study:

  • To investigate the role of SIRT1 in Pten-deficient murine thyroid and prostate carcinogenesis.
  • To determine the relationship between SIRT1 and c-MYC in cancer development.

Main Methods:

  • Transgenic mouse models with Sirt1 overexpression were used.
  • mRNA expression analysis and Western blotting were performed on murine tissues and cultured cells.
  • Correlation analysis was conducted between SIRT1 and c-MYC levels in human thyroid cancers.

Main Results:

  • Transgenic Sirt1 expression promoted thyroid and prostate carcinogenesis in Pten-deficient mice.
  • SIRT1 overexpression led to increased c-MYC transcription and protein levels in murine thyroid tumors.
  • SIRT1 was overexpressed in human thyroid cancers and positively correlated with c-MYC protein levels.
  • SIRT1 was found to stabilize c-MYC protein in cultured thyroid cancer cells.

Conclusions:

  • SIRT1 exhibits oncogenic activity in specific cancer contexts, contrary to previous assumptions.
  • SIRT1 promotes cancer progression by upregulating c-MYC.
  • SIRT1 represents a potential therapeutic target for thyroid carcinomas.