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Related Concept Videos

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...
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...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

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Related Experiment Video

Updated: May 10, 2026

Genome-Wide Mapping of Histone Modifications and Transcription Factor Binding Sites in Neuroendocrine Small Cell Lung Cancer Cell Lines Using CUT&RUN
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Localization, not important in all tumor-suppressing properties: a lesson learnt from scribble.

Imogen A Elsum1, Patrick O Humbert

  • 1Cell Cycle and Cancer Genetics, Research Division, Peter MacCallum Cancer Centre, Melbourne, Vic. 3002, Australia.

Cells, Tissues, Organs
|June 19, 2013
PubMed
Summary

Protein mislocalization in cancer is complex. Scribble protein

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Last Updated: May 10, 2026

Genome-Wide Mapping of Histone Modifications and Transcription Factor Binding Sites in Neuroendocrine Small Cell Lung Cancer Cell Lines Using CUT&RUN
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Comparative Lesions Analysis Through a Targeted Sequencing Approach
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Heterokaryon Technique for Analysis of Cell Type-specific Localization
09:31

Heterokaryon Technique for Analysis of Cell Type-specific Localization

Published on: March 11, 2011

Area of Science:

  • Cell Biology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Aberrant protein localization is implicated in epithelial cancers.
  • Few studies explore how protein mislocalization impacts specific cancer progression processes.
  • Scribble protein's tumor-suppressive role is linked to its localization.

Purpose of the Study:

  • To investigate how Scribble protein localization affects its tumor-suppressive properties.
  • To understand the impact of Scribble mislocalization on Ras-MAPK-induced transformation.

Main Methods:

  • Utilized a Scribble mutant (P305L) with cytosolic localization due to an LRR domain mutation.
  • Assessed the effects of wild-type and mutant Scribble on Ras-MAPK transformation phenotypes in vitro and in vivo.
  • Evaluated suppression of invasion, epithelial-to-mesenchymal transition, and anchorage-independent cell growth.

Main Results:

  • Scribble P305L mutant, localized in the cytosol, lost the ability to suppress Ras-MAPK-induced invasion.
  • The mislocalized Scribble mutant also failed to suppress epithelial-to-mesenchymal transition.
  • Cytosolic Scribble retained the ability to suppress anchorage-independent cell growth.

Conclusions:

  • Specific tumor-suppressive functions of Scribble are differentially sensitive to its cellular localization.
  • Protein mislocalization's contribution to cancer is multifaceted, affecting distinct biological processes.
  • Further research is needed to understand how cell polarity protein mislocalization drives cancer progression.