Loss of the Putative Tumor Suppressor Band 4.1B/Dal1 Gene Is Dispensable for Normal Development and Does Not Predispose to Cancer

Protein 4.1B suppresses prostate cancer progression and metastasis

“…Our parental PC-3 prostate cells expressed high levels of 4.1B and loss of this protein was only observed in aggressive variant cells (PC3-#82 and PC-3M) derived from this original starting population, suggesting that down-regulation of 4.1B enhanced the later stages of tumor progression to metastatic disease. Similarly, because genetic ablation of 4.1B in mice did not increase their predisposition to spontaneous tumor formation (15), but instead promoted the progression of prostatic tumor lesions already initiated by SV40, this observation again suggests that loss of 4.1B is important during the later stages of prostate tumorigenesis. In addition, as we have shown with the gene expression data set obtained from Lapointe et al (22), prostate tumors might down-regulate 4.1B expression relative to normal tissue early on and then further down-regulate expression during progression to metastatic disease.…”

“…We obtained 4.1B knockout mice (15) and confirmed the absence of this protein by performing Western blotting on brain and prostate lysates from 4.1B ϩ/ϩ or 4.1B Ϫ/Ϫ animals ( Fig. 3A).…”

“…However, these results were obtained from overexpression experiments conducted in vitro, and the putative role of 4.1B as a tumor suppressor in vivo has yet to be validated. In addition, 4.1B-deficient mice are healthy and do not develop spontaneous tumors above background levels (15).…”

Epigenetic Silencing of Cell Adhesion Molecule 1 in Different Cancer Progenitor Cells of Transgenic c-Myc and c-Raf Mouse Lung Tumors

“…Indeed, whereas Cadm1 expression decreased to nonexistent in the cell lines, Dal1 expression remarkably increased. A previous study generated mice deficient for Dal1 gene to elucidate its function in development and tumorigenesis (35). Dal1 null mice developed normally and were fertile.…”

A 130-kDa Protein 4.1B Regulates Cell Adhesion, Spreading, and Migration of Mouse Embryo Fibroblasts by Influencing Actin Cytoskeleton Organization

“…The 4.1B knock-out mice in a mixed background (38) were kindly provided by Dr. J. Kissil (The Wistar Institute). These mice were generated by targeting the second coding exon of the 4.1B locus, which contains sequences coding for ATG1 (38). The 4.1B knock-out mice were backcrossed onto C57BL/6 pure background for Ͼ10 generations.…”