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. 2009 Jun;3(2):153-7.
doi: 10.1007/s12079-009-0051-9. Epub 2009 Apr 28.

Alternative splicing of CCN mRNAs .... it has been upon us

Bernard Perbal  1
Affiliations

Alternative splicing of CCN mRNAs .... it has been upon us

Bernard Perbal. J Cell Commun Signal. 2009 Jun.

Abstract

Variant CCN proteins have been identified over the past decade in several normal and pathological situations. The production of CCN truncated proteins have been reported in the case of CCN2(ctgf), CCN3(nov), CCN4(wisp-1) and CCN6(wisp-3). Furthermore, the natural CCN5 is known to miss the C-terminal domain that is present in all other members of the CCN family of proteins. In spite of compelling evidence that assign important biological activities to these truncated CCN variants, their potential regulatory functions have only recently begun to be widely accepted. The report of CCN1(cyr61) intron 3 retention in breast cancer cells now confirms that, in addition to well documented post-translational processing of full length CCN proteins, alternative splicing is to be regarded as another effective way to generate CCN variants. These observations add to a previous bulk of evidence that support the existence of alternative splicing for other CCN genes. It has become clearly evident that we need to recognize these mechanisms as a means to increase the biological diversity of CCN proteins.

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Figures

Fig. 1
Fig. 1
Schematic organization of the various CCN spliced variants which have been described thus far. The prototypic structure of the CCN proteins (except fro CCN5 lacking CT) is represented on the top, with the five exons that encodes, the signal peptide (SP) and the Von Willebrand (VWC), thrombospondin (TSP1) and Cterminal (CT) domains (see Holbourn et al. 2008). Alternative splicing leading to variant proteins has been identified for CCN1 CCN4, CCN3. In the case of ccn1 and ccn4, the structure of the alternatively spliced messages has been established. Variant proteins resulting from alternative splicing have been identified in scirrhous gastric carcinoma (a), cholangiocarcinoma (b), HCS-2⁄8 human chondrosarcoma-derived chondrocytic cells (c), human hepatoma cells (d) Ewing’s tumors (e), human fibroblasts (f), Wilm’s tumors and normal human embryonic kidneys (g), human breast tumors (h). See text for details
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