Retraction: Suppression of intestinal tumorigenesis in Apc mutant mice upon Musashi-1 deletion. J. Cell Sci. doi: 10.1242/jcs.197574.

Expression of Concern: Suppression of intestinal tumorigenesis in Apc mutant mice upon Musashi-1 deletion. J. Cell Sci. doi: 10.1242/jcs.197574.

Suppression of intestinal tumorigenesis in Apc mutant mice upon Musashi-1 deletion.

Therapeutic strategies based on a specific oncogenic target are better justified when elimination of that particular oncogene reduces tumorigenesis in a model organism. One such oncogene, Musashi-1 (Msi-1), regulates translation of target mRNAs and is implicated in promoting tumorigenesis in the colon and other tissues. Msi-1 targets include the tumor suppressor adenomatous polyposis coli (Apc)...

Retraction: Eya1 protein phosphatase regulates tight junction formation in lung distal epithelium. J. Cell. Sci. doi: 10.1242/102848.

The journal is retracting ‘Eya1 protein phosphatase regulates tight junction formation in lung distal epithelium’ by Ahmed H. K. ElHashash, Gianluca Turcatel, Saaket Varma, Mohamed Berika, Denise Al Alam and David Warburton (2012). J. Cell Sci. 125, 4036-4048 (doi: 10.1242/102848). Journal of Cell Science is retracting this article at the request of the institution. The authors have been notifi...

The overexpression of the putative gut stem cell marker Musashi-1 induces tumorigenesis through Wnt and Notch activation.

The RNA-binding protein Musashi-1 (Msi1) has been proposed as a marker of intestinal epithelial stem cells. These cells are responsible for the continuous renewal of the intestinal epithelium. Although the function of Msi1 has been studied in several organs from different species and in mammalian cell lines, its function and molecular regulation in mouse intestinal epithelium progenitor cells a...

Deficiency of the LIM-Only Protein FHL2 Reduces Intestinal Tumorigenesis in Apc Mutant Mice

BACKGROUND The four and a half LIM-only protein 2 (FHL2) is capable of shuttling between focal adhesion and nucleus where it signals through direct interaction with a number of proteins including beta-catenin. Although FHL2 activation has been found in various human cancers, evidence of its functional contribution to carcinogenesis has been lacking. METHODOLOGY/PRINCIPAL FINDINGS Here we have...