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Bin1 Ablation Increases Susceptibility to Cancer during Aging, Particularly Lung Cancer

Chang, Mee Young, Boulden, Janette, Katz, Jessica B., Wang, Liwei, Meyer, Thomas J., Soler, Alejandro Peralta, Muller, Alexander J., Prendergast, George C.·2007·Cancer Research
DOI 10.1158/0008-5472.can-07-1100

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Abstract

Age is the major risk factor for cancer, but few genetic pathways that modify cancer incidence during aging have been described. Bin1 is a prototypic member of the BAR adapter gene family that functions in vesicle dynamics and nuclear processes. Bin1 limits oncogenesis and is often attenuated in human cancers, but its role in cancer suppression has yet to be evaluated fully in vivo. In the mouse, homozygous deletion of Bin1 causes developmental lethality, so to assess this role, we examined cancer incidence in mosaic null mice generated by a modified Cre-lox technology. During study of these animals, one notable phenotype was an extended period of female fecundity during aging, with mosaic null animals retaining reproductive capability until the age of 17.3 ± 1.1 months. Through 1 year of age, cancer incidence was unaffected by Bin1 ablation; however, by 18 to 20 months of age, ∼50% of mosaic mice presented with lung adenocarcinoma and ∼10% with hepatocarcinoma. Aging mosaic mice also displayed a higher incidence of inflammation and/or premalignant lesions, especially in the heart and prostate. In mice where colon tumors were initiated by a ras-activating carcinogen, Bin1 ablation facilitated progression to more aggressive invasive status. In cases of human lung and colon cancers, immunohistochemical analyses evidenced frequent attenuation of Bin1 expression, paralleling observations in other solid tumors. Taken together, our findings highlight an important role for Bin1 as a negative modifier of inflammation and cancer susceptibility during aging. [Cancer Res 2007;67(16):7605–12]

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  1. Sakamuro D, Elliott K, Wechsler-Reya R, Prendergast GC. BIN1 is a novel MYC-interacting protein with features of a tumor suppressor. Nat Genet 1996; 14: 69–77. · DOI · Paper page
  2. Elliott K, Sakamuro D, Basu A, et al. Bin1 functionally interacts with Myc in cells and inhibits cell proliferation by multiple mechanisms. Oncogene 1999; 18: 3564–73. · DOI
  3. Pineda-Lucena A, Ho CS, Mao DY, et al. A structure-based model of the c-Myc/Bin1 protein interaction shows alternative splicing of Bin1 and c-Myc phosphorylation are key binding determinants. J Mol Biol 2005; 351: 182–94. · DOI
  4. Deming SL, Nass SJ, Dickson RB, Trock BJ. C-myc amplification in breast cancer: a meta-analysis of its occurrence and prognostic relevance. Br J Cancer 2000; 83: 1688–95. · DOI
  5. Ramjaun AR, Micheva KD, Bouchelet I, McPherson PS. Identification and characterization of a nerve terminal-enriched amphiphysin isoform. J Biol Chem 1997; 272: 16700–6. · DOI · Paper page
  6. Tsutsui K, Maeda Y, Tsutsui K, Seki S, Tokunaga A. cDNA cloning of a novel amphiphysin isoform and tissue-specific expression of its multiple splice variants. Biochem Biophys Res Commun 1997; 236: 178–83. · DOI · Paper page
  7. Wechsler-Reya R, Sakamuro D, Zhang J, Duhadaway J, Prendergast GC. Structural analysis of the human BIN1 gene: evidence for tissue-specific transcriptional regulation and alternate RNA splicing. J Biol Chem 1997; 272: 31453–8. · DOI · Paper page
  8. Ren G, Vajjhala P, Lee JS, Winsor B, Munn AL. The BAR domain proteins: molding membranes in fission, fusion, and phagy. Microbiol Mol Biol Rev 2006; 70: 37–120. · DOI
  9. Miaczynska M, Christoforidis S, Giner A, et al. APPL proteins link Rab5 to nuclear signal transduction via an endosomal compartment. Cell 2004; 116: 445–56. · DOI
  10. Ge K, DuHadaway J, Du W, Herlyn M, Rodeck U, Prendergast GC. Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma. Proc Natl Acad Sci U S A 1999; 96: 9689–94. · DOI
  11. Ge K, DuHadaway J, Sakamuro D, Wechsler-Reya R, Reynolds C, Prendergast GC. Losses of the tumor suppressor Bin1 in breast carcinoma are frequent and reflect deficits in a programmed cell death capacity. Int J Cancer 2000; 85: 376–83. · DOI
  12. Ge K, Minhas F, DuHadaway J, et al. Loss of heterozygosity and tumor suppressor activity of Bin1 in prostate carcinoma. Int J Cancer 2000; 86: 155–61. · DOI
  13. DuHadaway JB, Sakamuro D, Ewert DL, Prendergast GC. Bin1 mediates apoptosis by c-Myc in transformed primary cells. Cancer Res 2001; 16: 3151–6.
  14. Muller AJ, DuHadaway JB, Donover PS, Sutanto-Ward E, Prendergast GC. Targeted deletion of the suppressor gene Bin1/amphiphysin 2 enhances the malignant character of transformed cells. Cancer Biol Ther 2004; 3: 1236–42. · DOI
  15. Tajiri T, Liu X, Thompson PM, et al. Expression of a MYCN-interacting isoform of the tumor suppressor BIN1 is reduced in neuroblastomas with unfavorable biological features. Clin Cancer Res 2003; 9: 3345–55.
  16. Xu Q, Lee C. Discovery of novel splice forms and functional analysis of cancer-specific alternative splicing in human expressed sequences. Nucleic Acids Res 2003; 31: 5635–43. · DOI
  17. Karni R, de Stanchina E, Lowe SW, Sinha R, Mu D, Krainer AR. The gene encoding the splicing factor SF2/ASF is a proto-oncogene. Nat Struct Mol Biol 2007; 14: 185–93. · DOI
  18. Muller AJ, Baker JF, DuHadaway JB, et al. Targeted disruption of the murine Bin1/amphiphysin II gene does not disable endocytosis but results in embryonic cardiomyopathy with aberrant myofibril formation. Mol Cell Biol 2003; 23: 4295–306. · DOI · Paper page
  19. Chang MY, Boulden J, Sutanto-Ward E, et al. Bin1 ablation in mammary gland delays tissue remodeling and drives cancer progression. Cancer Res 2007; 67: 100–7. · DOI
  20. Mao NC, Steingrimsson E, DuHadaway J, et al. The murine Bin1 gene functions early in myogenesis and defines a new region of synteny between mouse chromosome 18 and human chromosome 2. Genomics 1999; 56: 51–8. · DOI
  21. Jackson PE, Cooper DP, O'Connor PJ, Povey AC. The relationship between 1,2-dimethylhydrazine dose and the induction of colon tumours: tumour development in female SWR mice does not require a K-ras mutational event. Carcinogenesis 1999; 20: 509–13. · DOI
  22. Lakso M, Pichel JG, Gorman JR, et al. Efficient in vivo manipulation of mouse genomic sequences at the zygote stage. Proc Natl Acad Sci U S A 1996; 93: 5860–5. · DOI · Paper page
  23. Dooley TP, Miranda M, Jones NC, DePamphilis ML. Transactivation of the adenovirus EIIa promoter in the absence of adenovirus E1A protein is restricted to mouse oocytes and preimplantation embryos. Development 1989; 107: 945–56. · DOI
  24. Lerner SP, Anderson CP, Walford RL, Finch CE. Genotypic influences on reproducing aging of inbred female mice: effects of H-2 and non–H2 alleles. Biol Reprod 1988; 38: 1035–43. · DOI
  25. DuHadaway JB, Lynch FJ, Brisbay S, et al. Immunohistochemical analysis of Bin1/amphiphysin II in human tissues: diverse sites of nuclear expression and losses in prostate cancer. J Cell Biochem 2003; 88: 635–42. · DOI · Paper page
  26. Reddy JK, Rao MS. Lipid metabolism and liver inflammation. II. Fatty liver disease and fatty acid oxidation. Am J Physiol Gastrointest Liver Physiol 2006; 290: G852–8. · DOI
  27. Jackson-Grusby L. Modeling cancer in mice. Oncogene 2002; 21: 5504–14. · DOI
  28. Dragani TA. 10 years of mouse cancer modifier loci: human relevance. Cancer Res 2003; 63: 3011–8.
  29. Perrimon N. Creating mosaics in Drosophila. Int J Dev Biol 1998; 42: 243–7.
  30. Betz UA, Vosshenrich CA, Rajewsky K, Muller W. Bypass of lethality with mosaic mice generated by Cre-loxP–mediated recombination. Curr Biol 1996; 6: 1307–16. · DOI
  31. Kwan KM. Conditional alleles in mice: practical considerations for tissue-specific knockouts. Genesis 2002; 32: 49–62. · DOI
  32. Routhier EL, Donover PS, Prendergast GC. hob1+, the homolog of Bin1 in fission yeast, is dispensable for endocytosis but required for the response to starvation or genotoxic stress. Oncogene 2003; 22: 637–48. · DOI
  33. Munn DH, Mellor AL. Indoleamine 2,3-dioxygenase and tumor-induced tolerance. J Clin Invest 2007; 117: 1147–54. · DOI
  34. Munn DH, Zhou M, Attwood JT, et al. Prevention of allogeneic fetal rejection by tryptophan catabolism. Science 1998; 281: 1191–3. · DOI
  35. Jung M, Poepping I, Perrot A, et al. Investigation of a family with autosomal dominant dilated cardiomyopathy defines a novel locus on chromosome 2q14-22. Am J Hum Genet 1999; 65: 1068–77. · DOI
  36. Zhou H, Liu L, Lee K, et al. Lung tumorigenesis associated with erb-B-2 and erb-B-3 overexpression in human erb-B-3 transgenic mice is enhanced by methylnitrosourea. Oncogene 2002; 21: 8732–40. · DOI
  37. Ghaneie A, Zemba-Palko V, Itoh H, et al. Bin1 attenuation in breast cancer is correlated to nodal metastasis and reduced survival. Cancer Biol Ther 2007; 6: 192–4. · DOI

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Metadata

Authors
Chang, M. Y., Boulden, J., Katz, J. B., Wang, L., Meyer, T. J., Soler, A. P., Muller, A. J., & Prendergast, G. C.
Affiliations
  • 1Lankenau Institute for Medical Research, and
  • 3Department of Gastrointestinal Medical Oncology, M. D. Anderson Cancer Center, Houston, Texas;
  • 2Lung Cancer Program, Lankenau Hospital, Wynnewood, Pennsylvania;
Venue
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2007-08-15
Volume
67
Issue
16
Pages
7605-7612
ISSN
  • 0008-5472
  • 1538-7445
DOI
10.1158/0008-5472.can-07-1100
Cited by
67
References
4
Language
en

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