Loss of the putative tumor suppressor band 4.1B/Dal1 gene is dispensable for normal development and does not predispose to cancer.

Document Type

Article

Publication Date

2005

Keywords

Animals, Apoptosis, Blotting-Southern, Blotting-Western, Brain, Cell-Death, Cell-Proliferation, Cells-Cultured, Cloning-Molecular, Cytoskeletal-Proteins, DNA-Primers, Female, Genetic-Predisposition-to-Disease, Genotype, Immunohistochemistry, Kinetics, Lung, Mammary-Glands-Animal, Membrane-Proteins, Mice-Knockout, Mice-Transgenic, Models-Genetic, Mutation, Neoplasms, Polymerase-Chain-Reaction

First Page

10052

Last Page

10059

JAX Source

Mol Cell Biol 2005 Nov; 25(22):10052-9.

Abstract

The band 4.1 proteins are cytoskeletal proteins, harboring a conserved FERM domain highly homologous to the N-terminal FERM domain of ezrin, radixin, moesin, and merlin. Recently, a truncated form of the 4.1B protein, termed Dal-1, was identified in a screen as down regulated in adenocarcinoma of the lung and was mapped to chromosome 18p11.3, which is lost in 38% of primary non-small cell lung carcinoma tumors. Analysis of several meningiomas has shown that Dal-1 expression was lost in 76% of the tumors. To further elucidate the function of the 4.1B/Dal-1 gene in development and tumorigenesis we generated mice deficient for this allele. The 4.1B/Dal-1 null mice develop normally and are fertile. Rates of cellular proliferation and apoptosis in brain, mammary, and lung tissues from the 4.1B/Dal-1 null mice were indistinguishable from those seen with wild-type mice. Aging studies indicate that these mice do not have a propensity to develop tumors. Analysis of fibroblasts from these mice demonstrated that the growth characteristics and kinetics of these cells were not different from those of cells from the wild-type mice. These findings indicate that the 4.1B gene is not required for normal development and that 4.1B/Dal-1 does not function as a tumor suppressor gene.

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