New function of protein involved in colon cancer identified

IDIBELL and ICO researchers have participated in an international study of gene transcription by phosphorylation of specific substrates related to cancer progression and metastasis. This research was published this week in the scientific journal Cell Reports.

The study, led by researchers from the Hospital del Mar Medical Research Institute (IMIM) and also participated by the researchers Alberto Villanueva and Maria Martinez, from the Chemoresistance and Predictive Factors to Tumour Response and

Stromal Microenvironment from the IDIBELL and ICO, has determined the function of a new variant of the enzyme IKKalpha (IKKα) in the activation of some of the genes involved in tumor progression of colorectal cancer.

The research group, in order to increase the knowledge of mechanics between tumorgenesis and IKKα activity, analyzed 288 human colorectal cancer samples and found a significant association between the presence of nuclear IKK and malignancy. It was shown that nuclear IKKα regulates gene transcription by phosphorylating specific substrates, which is associated with cancer progression and metastasis. Importantly, the nucleus of tumor cells contains an active IKKα isoform with a predicted molecular weight of 45 kDa (p45-IKKα).

In most samples of human colon cancer was identified the presence of P45-IKKα. It was demonstrated that specific blocking of this new form of IKKα prevents the growth of this particular cancer cells. The results could mean advance for the design of new drugs to inhibit this enzyme effectively and be less toxic to the rest of body cells.

Reference of the paper: A Truncated Form of IKKα Is Responsible for Specific Nuclear IKK Activity in Colorectal Cancer. Pol Margalef, Vanessa Fernández-Majada, Alberto Villanueva, Ricard Garcia-Carbonell, Mar Iglesias, Laura López, María Martínez-Iniesta, Jordi Villà-Freixa, Mari Carmen Mulero, Montserrat Andreu, Ferran Torres, Marty W. Mayo, Anna Bigas, Lluis Espinosa. Cell Reports 2, 1-15, October 25, 2012.

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