This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yi, C. Articles by Kissil, J. L. Search for Related Content PubMed PubMed Citation Articles by Yi, C. Articles by Kissil, J. L.

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

Chunling Yi,¹ Joseph H. McCarty,^2, Scott A. Troutman,¹ Matthew S. Eckman,² Roderick T. Bronson,³ and Joseph L. Kissil^1*

Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, Pennsylvania,¹ Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts,² Department of Pathology, Tufts University School of Medicine and Veterinary Medicine, Boston, Massachusetts 02111³

Received 17 June 2005/ Returned for modification 11 July 2005/ Accepted 23 August 2005

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.

Present address: Department of Cancer Biology, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030.

This article has been cited by other articles:

• Wong, S. Y., Haack, H., Kissil, J. L., Barry, M., Bronson, R. T., Shen, S. S., Whittaker, C. A., Crowley, D., Hynes, R. O. (2007). Protein 4.1B suppresses prostate cancer progression and metastasis. Proc. Natl. Acad. Sci. USA 104: 12784-12789 [Abstract] [Full Text]