A relationship between cancer genes and the reprogramming gene SOX2 discovered

December 06, 2012

A team of researchers from the Spanish National Cancer Research Centre (CNIO), led by Manuel Serrano, from the Tumour Suppression Group, together with scientists from London and Santiago de Compostela, has discovered that the cellular reprogramming gene SOX2, which is involved in several types of cancers, such as lung cancer and pituitary cancer, is directly regulated by the tumor suppressor CDKN1B(p27) gene, which is also associated with these types of cancer.

The same edition of the online version of the journal also includes a study led by Massimo Squatrito, who recently joined the CNIO to direct the Seve Ballesteros Foundation Brain Tumour Group. This study, carried out in Eric C. Holland's laboratory, at the Memorial Sloan Kettering Cancer Center (MSKCC), in Nueva York, shows the relationship between MEF, a gene regulator involved glioblastomas - the most aggressive and common brain tumours -, and SOX2.

YAMANAKA'S CELLULAR REPROGRAMMING CONTINUES TO SURPRISE

The cell reprogramming process, discovered by this year's Nobel Prize winner, Shinya Yamanaka, has become a powerful tool for researchers. Via the introduction of a cocktail of four genes into cells, among them SOX2, scientists can reprogram cells and transform them into stem cells which can be used to study a variety of processes, including cancer.

The research team led by Manuel Serrano and Manuel Collado was interested in the possible role of the tumour suppressor gene CDKN1B(p27) in reprogramming. During the course of these studies, Han Li, first author of the study, unexpectedly discovered that cells deficient in the CDKN1B(p27) gene could be reprogrammed without the need to introduce SOX2. This observation was the starting point to unravel the functional relationship between both genes.

The work led by Squatrito, in which the researcher Elena Bazzoli figures as first author, was based on earlier works that linked SOX2 with tumorigenesis. The article describes how SOX2 is regulated by MEF in cells of the nervous system. "Brain tumour cells acquire stem cell traits thanks to the participation of SOX2, and this produces an increase in tumorigenic potential" states Squatrito.

These new insights help to understand the origin of cancers linked to CDKN1B(p27) and MEF, and highlight the potential role of adult stem cells in cancer.
-end-
Reference articles:

p27Kip1 directly represses Sox2 during embryonic stem cell differentiation. Han Li, Manuel Collado, Aranzazu Villasante, Ander Matheu, Cian J. Lynch, Marta Cañamero, Karine Rizzoti, Carmen Carneiro, Gloria Martínez, Anxo Vidal, Robin Lovell-Badge, Manuel Serrano. Cell Stem Cell (2012). doi: 10.1016/j.stem.2012.09.014

MEF Promotes Stemness in the Pathogenesis of Gliomas. Elena Bazzoli, Teodoro Pulvirenti, Moritz C. Oberstadt, Fabiana Perna, Boyoung Wee, Nikolaus Schultz, Jason T. Huse, Elena I. Fomchenko, Francesca Voza, Viviane Tabar, Cameron W. Brennan, Lisa M. DeAngelis, Stephen D. Nimer, Eric C. Holland, Massimo Squatrito. Cell Stem Cell (2012). doi: 10.1016/j.stem.2012.09.012

Centro Nacional de Investigaciones Oncológicas (CNIO)

Related Stem Cells Articles from Brightsurf:

SUTD researchers create heart cells from stem cells using 3D printing
SUTD researchers 3D printed a micro-scaled physical device to demonstrate a new level of control in the directed differentiation of stem cells, enhancing the production of cardiomyocytes.

More selective elimination of leukemia stem cells and blood stem cells
Hematopoietic stem cells from a healthy donor can help patients suffering from acute leukemia.

Computer simulations visualize how DNA is recognized to convert cells into stem cells
Researchers of the Hubrecht Institute (KNAW - The Netherlands) and the Max Planck Institute in Münster (Germany) have revealed how an essential protein helps to activate genomic DNA during the conversion of regular adult human cells into stem cells.

First events in stem cells becoming specialized cells needed for organ development
Cell biologists at the University of Toronto shed light on the very first step stem cells go through to turn into the specialized cells that make up organs.

Surprising research result: All immature cells can develop into stem cells
New sensational study conducted at the University of Copenhagen disproves traditional knowledge of stem cell development.

The development of brain stem cells into new nerve cells and why this can lead to cancer
Stem cells are true Jacks-of-all-trades of our bodies, as they can turn into the many different cell types of all organs.

Healthy blood stem cells have as many DNA mutations as leukemic cells
Researchers from the Princess Máxima Center for Pediatric Oncology have shown that the number of mutations in healthy and leukemic blood stem cells does not differ.

New method grows brain cells from stem cells quickly and efficiently
Researchers at Lund University in Sweden have developed a faster method to generate functional brain cells, called astrocytes, from embryonic stem cells.

NUS researchers confine mature cells to turn them into stem cells
Recent research led by Professor G.V. Shivashankar of the Mechanobiology Institute at the National University of Singapore and the FIRC Institute of Molecular Oncology in Italy, has revealed that mature cells can be reprogrammed into re-deployable stem cells without direct genetic modification -- by confining them to a defined geometric space for an extended period of time.

Researchers develop a new method for turning skin cells into pluripotent stem cells
Researchers at the University of Helsinki, Finland, and Karolinska Institutet, Sweden, have for the first time succeeded in converting human skin cells into pluripotent stem cells by activating the cell's own genes.

Read More: Stem Cells News and Stem Cells Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.