A novel oncogenic BTK isoform is overexpressed in colon cancers and required for RAS-mediated transformation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-01-25

AUTHORS

E Grassilli, F Pisano, A Cialdella, S Bonomo, C Missaglia, M G Cerrito, L Masiero, L Ianzano, F Giordano, V Cicirelli, R Narloch, F D'Amato, B Noli, G L Ferri, B E Leone, G Stanta, S Bonin, K Helin, R Giovannoni, M Lavitrano

ABSTRACT

Bruton's tyrosine kinase (BTK) is essential for B-cell proliferation/differentiation and it is generally believed that its expression and function are limited to bone marrow-derived cells. Here, we report the identification and characterization of p65BTK, a novel isoform abundantly expressed in colon carcinoma cell lines and tumour tissue samples. p65BTK protein is expressed, through heterogeneous nuclear ribonucleoprotein K (hnRNPK)-dependent and internal ribosome entry site-driven translation, from a transcript containing an alternative first exon in the 5'-untranslated region, and is post-transcriptionally regulated, via hnRNPK, by the mitogen-activated protein kinase (MAPK) pathway. p65BTK is endowed with strong transforming activity that depends on active signal-regulated protein kinases-1/2 (ERK1/2) and its inhibition abolishes RAS transforming activity. Accordingly, p65BTK overexpression in colon cancer tissues correlates with ERK1/2 activation. Moreover, p65BTK inhibition affects growth and survival of colon cancer cells. Our data reveal that BTK, via p65BTK expression, is a novel and powerful oncogene acting downstream of the RAS/MAPK pathway and suggest that its targeting may be a promising therapeutic approach. More... »

PAGES

4368-4378

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2015.504

DOI

http://dx.doi.org/10.1038/onc.2015.504

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043263135

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26804170


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