분자유전학실험실 (단국대학교 분자생물학과)



 관리자 ( 2010-11-02 10:08:37 , Hit : 3892
 Too Much SP2 Protein Turns Stem Cells Into “Evil Twin” Tumor-forming Cancer Cells

Too Much SP2 Protein Turns Stem Cells Into “Evil Twin” Tumor-forming Cancer Cells
For Immediate Release
Tracey Peake | News Services | 919.515.6142

Release Date: October 27, 2010
Filed under Facebook, Releases

Researchers at North Carolina State University have found that the overproduction of a key protein in stem cells causes those stem cells to form cancerous tumors. Their work may lead to new treatments for a variety of cancers.

Dr. Jon Horowitz, associate professor of molecular biomedical sciences, and a team of NC State researchers looked at the protein SP2, which regulates the activity of other genes. They knew that elevated amounts of SP2 had been observed in human prostate-cancer patients, and that these levels only increased as the tumors became more dangerous. They then showed that precisely the same thing occurs in mouse skin tumors.

Horowitz and the team decided to look at SP2 as a possible cause of tumor formation in epithelial cell-derived tumors, which comprise about 80 percent of all human tumors; epithelial cells cover the body’s internal and external surfaces. They found that overproduction of the SP2 protein in epithelial stem cells stopped them from spawning mature descendants. The affected stem cells, unable to produce mature cells, just kept proliferating, resulting in the formation of tumors.

The researchers’ results are published in the Nov. 3 edition of the journal Cancer Research.

“Something happens to normal stem cells that changes the way SP2 is regulated, and it starts being overproduced,” Horowitz says. “SP2 basically hijacks the stem cell, and turns it into its evil twin – a cancer cell.”

Now that the link between tumor formation and SP2 has been shown, Horowitz says, scientists can turn their attention to looking at ways to target the overproduction of this protein. “Our hope is that we can find an ‘antidote’ to SP2, to restore normal cell proliferation to those cancer stem cells and reverse the process.”

The research was funded by a grant from the National Institutes of Health (NIH). The Department of Molecular Biomedical Sciences is part of NC State’s College of Veterinary Medicine.

-peake-

Note to editors: Abstract of the paper follows.

“Overexpression of Transcription Factor Sp2 Inhibits Epidermal Differentiation and Increases Susceptibility to Wound and Carcinogen-Induced Tumorigenesis”
Authors: Tae-Hyung Kim, Shannon L. Chiera, Keith E. Linder, Robert C. Smart, and Jonathan M. Horowitz, NC State University; Carol S. Trempus, Metabolism and Molecular Mechanisms Group, Laboratory of Toxicology and Pharmacology, NIH, NIEHS
Published: Nov. 3 in Cancer Research

Abstract: Sp proteins are evolutionarily-conserved transcription factors required for the expression of a wide variety of genes that are critical for development and cell-cycle progression. De-regulated expression of certain Sp proteins is associated with the formation of a variety of human tumors, however direct evidence that any given Sp protein is oncogenic has been lacking. Here we report that Sp2 protein abundance in mice increases in concert with the progression of carcinogen-induced murine squamous cell carcinomas. Transgenic mice specifically overexpressing murine Sp2 in epidermal basal keratinocytes were highly susceptible to wound- and carcinogen-induced papillomagenesis. Transgenic animals that were homozygous rather than hemizygous for the Sp2 transgene exhibited a striking arrest in the epidermal differentiation program, perishing within two weeks of birth. Our results directly support the likelihood that Sp2 overexpression occurring in various human cancers has significant functional impact.









807   First Clinical Trial of Gene Therapy for Muscular Dystrophy Lends Insight Into the Disease  이성욱 2010/10/11 2565
806   Hepatitis C virus infection linked to fat enzyme in liver cells  이성욱 2010/10/14 3211
805   Hepatitis C Virus Infection Linked to Fat Enzyme in Liver Cells  이성욱 2010/10/15 2976
804   Roche hepatitis C drug appears safe in combination  이성욱 2010/10/17 3000
803   헤르페스 감염 메커니즘 밝혀져  이성욱 2010/10/17 5887
802   Study points to possible gene therapy for depression  이성욱 2010/10/22 2497
801   More than a chicken, fewer than a grape - Exact tally of human genes remains elusive  이성욱 2010/10/25 2563
800   Strides Against Hepatitis C Open Door to Blockbusters  이성욱 2010/11/02 2567
799   Black patients fare well on Vertex hepatitis C drug  이성욱 2010/11/02 2712
  Too Much SP2 Protein Turns Stem Cells Into “Evil Twin” Tumor-forming Cancer Cells  관리자 2010/11/02 3892
797   NC State Develops More Precise Genetic ‘Off Switches’  이성욱 2010/11/03 2633
796   Breakthrough in cancer vaccine research  이성욱 2010/11/08 2685
795   DNA sequence may be lost in translation  이성욱 2010/11/10 2788
794   Lung Cancer in Smokers, Nonsmokers May Be a Different Disease  이성욱 2010/11/10 2576
793   Why brain tumors hard to treat  이성욱 2010/11/23 2918
792   Vertex submits application for hepatitis C drug  이성욱 2010/11/25 3431
791   Tumours grow their own blood vessels  이성욱 2010/11/25 2359
790   Top 5 papers of 2010  이성욱 2010/12/10 2327
789   Microbe gets toxic response  이성욱 2010/12/10 2469
788   Basel Declaration defends animal research  이성욱 2010/12/10 2371

[이전 10개] [1]..[21][22][23] 24 [25][26][27][28][29][30]..[64] [다음 10개]
 

Copyright 1999-2024 Zeroboard / skin by ROBIN