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Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...

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In Vitro Establishment of a Genetically Engineered Murine Head and Neck Cancer Cell Line using an Adeno-Associated Virus-Cas9 System
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Stem cell gene expression changes induced specifically by mutated K-ras.

Feijun Luo1, Rifat Hamoudi, David G Brooks

  • 1Department of Pathology, Addenbrooke's Hospital, Hills Road, University of Cambridge, Cambridge CB2 2QQ, UK.

Gene Expression
|February 9, 2008
PubMed
Summary
This summary is machine-generated.

Mutated K-ras (K-ras(Val12)) in stem cells drives cancer-related changes, including increased proliferation and altered differentiation. This study reveals key gene expression shifts linked to these neoplastic alterations.

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Area of Science:

  • Molecular Biology
  • Stem Cell Biology
  • Oncology

Background:

  • K-Ras proteins are crucial for cell signaling, regulating stem cell functions like proliferation, apoptosis, and differentiation.
  • The role of mutated K-Ras in cancer development, particularly in stem cells, remains incompletely understood.

Purpose of the Study:

  • To investigate the specific gene expression changes induced by mutated K-ras (K-ras(Val12)) in normal stem cells.
  • To correlate these gene expression alterations with phenotypic changes relevant to neoplasia.

Main Methods:

  • Utilized cDNA microarrays to compare gene expression profiles of wild-type murine embryonic stem (ES) cells and ES cells expressing K-ras(Val12).
  • Validated array data using real-time quantitative PCR in ES cells and K-ras(Val12) transgenic mouse intestinal tissues.

Main Results:

  • K-ras(Val12) expression enhanced ES cell self-renewal, increased proliferation, and heightened susceptibility to DNA damage-induced apoptosis.
  • Observed upregulation of cell growth and DNA-associated proteins, along with specific apoptosis-related proteins.
  • Downregulation of structural proteins, extracellular matrix components, and receptors indicated a less differentiated phenotype.

Conclusions:

  • Mutated K-ras significantly alters stem cell gene expression, promoting phenotypes associated with neoplasia.
  • These findings provide molecular insights into how K-Ras mutations contribute to tumor initiation and progression in stem cells.