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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...
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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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...
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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

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Related Experiment Video

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Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs
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YAP1 meets tumor suppression.

Sabrina Strano1, Giovanni Blandino

  • 1Department of Experimental Oncology, Regina Elena Cancer Institute, Via delle Messi d'oro, 156, 00158-Rome, Italy.

Molecular Cell
|September 25, 2007
PubMed
Summary

The study reveals that RASSF1A triggers apoptosis by activating YAP1, a transcriptional coactivator. This process involves YAP1 moving to the nucleus and binding with p73, crucial for cell death.

Area of Science:

  • Molecular biology
  • Cellular processes
  • Cancer research

Background:

  • Apoptosis, or programmed cell death, is vital for development and tissue homeostasis.
  • Dysregulation of apoptosis is implicated in various diseases, including cancer.
  • The RASSF1A tumor suppressor and YAP1 transcriptional coactivator play roles in cell fate.

Purpose of the Study:

  • To elucidate the molecular mechanism by which RASSF1A induces apoptosis.
  • To investigate the role of the transcriptional coactivator YAP1 in RASSF1A-mediated cell death.
  • To determine the interaction between RASSF1A, YAP1, and p73 in the apoptosis pathway.

Main Methods:

  • Cell culture and transfection techniques.
  • Western blotting and immunoprecipitation assays to detect protein interactions.

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In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
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In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

Published on: July 25, 2019

  • RNA interference (RNAi) to silence RASSF1A expression in tumor cells.
  • Analysis of nuclear translocation and p73 binding of YAP1.

    • Main Results:

    • RASSF1A induces apoptosis through a pathway involving the transcriptional coactivator YAP1.
    • YAP1 translocates to the nucleus and binds to p73, facilitating the execution of apoptosis.
    • Silencing of RASSF1A in tumors inhibits YAP1-p73-dependent apoptosis, highlighting its critical role.

    Conclusions:

    • RASSF1A-induced apoptosis is dependent on the nuclear translocation and p73-binding activity of YAP1.
    • The RASSF1A-YAP1-p73 axis represents a key pathway for tumor suppressor-mediated cell death.
    • Targeting this pathway may offer therapeutic strategies for cancer treatment.