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Related Concept Videos

Forced Transdifferentiation01:28

Forced Transdifferentiation

Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
Artificial transdifferentiation occurs...
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...
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 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.
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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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Transdifferentiation-inducing HCCR-1 oncogene.

Seon-Ah Ha1, Hyun K Kim, JinAh Yoo

  • 1Molecular Genetic Laboratory, Catholic Medical Research Institute, The Catholic University of Korea, Seoul, Korea.

BMC Cell Biology
|July 2, 2010
PubMed
Summary

HCCR-1 drives cell transdifferentiation, including epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET). This suggests HCCR-1 may regulate tissue development and cancer progression.

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Area of Science:

  • Cell biology
  • Developmental biology
  • Cancer research

Background:

  • Cellular phenotypes are plastic and can change through transdifferentiation.
  • The differentiated state of cells is not fixed and can be altered by molecular signals.

Purpose of the Study:

  • To investigate the role of HCCR-1 in cell transdifferentiation.
  • To explore HCCR-1's potential involvement in cancer stem cell transdifferentiation and tissue morphogenesis.

Main Methods:

  • Investigated HCCR-1's effect on epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) in human and mouse cells.
  • Observed expression of HCCR-1 during embryonic kidney development.

Main Results:

  • HCCR-1 induces EMT in human cells and MET in mouse cells.
  • CD117/c-Kit, a stem cell factor receptor, was upregulated in HCCR-1-induced transdifferentiated sarcoma tissues.
  • HCCR-1 expression was detected during embryonic kidney development, similar to MET.

Conclusions:

  • HCCR-1 acts as a key regulator in cell transdifferentiation processes.
  • HCCR-1 may play a role in stimulating epithelial or mesenchymal morphogenesis during neoplastic transformation.