The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Transforming Growth Factor β Receptor Type II Inactivation Induces the Malignant Transformation of Intestinal Neoplasms Initiated by Apc Mutation
Abstract
The transforming growth factor-β (TGF-β) signaling pathway is a tumor-suppressor pathway that is commonly inactivated in colon cancer. TGF-β is a secreted ligand that mediates its effects through a transmembrane heteromeric receptor complex, which consists of type I (TGFBR1) and type II subunits (TGFBR2). Approximately 30% of colon cancers carry TGFBR2 mutations, demonstrating that it is a common target for mutational inactivation in this cancer. To assess the functional role of TGFBR2 inactivation in the multistep progression sequence of colon cancer, we generated a mouse model that recapitulates two common genetic events observed in human colon cancer by mating Apc1638N/wt mice with mice that are null for Tgfbr2 in the intestinal epithelium, Villin-Cre;Tgfbr2E2flx/E2flx mice. In this model, we observed a dramatic increase in the number of intestinal adenocarcinomas in the Apc1638N/wt;Villin-Cre;Tgfbr2E2flx/E2flx mice (called Apc1638N/wt;Tgfbr2IEKO) compared with those mice with intact Tgfbr2 (Apc1638N/wt;Tgfbr2E2flx/E2flx). Additionally, in vitro analyses of epithelial tumor cells derived from the Apc1638N/wt;Tgfbr2IEKO mice showed enhanced expression and activity of matrix metalloproteinase MMP-2 and MMP-9, as well as increased TGF-β1 secretion in the conditioned medium. Similarly, primary tumor tissues from the Apc1638N/wt;Tgfbr2IEKO mice also showed elevated amounts of TGF-β1 as well as higher MMP-2 activity in comparison with Apc1638N/wt;Tgfbr2E2flx/E2flx–derived tumors. Thus, loss of TGFBR2 in intestinal epithelial cells promotes the invasion and malignant transformation of tumors initiated by Apc mutation, providing evidence that Wnt signaling deregulation and TGF-β signaling inactivation cooperate to drive the initiation and progression, respectively, of intestinal cancers in vivo. (Cancer Res 2006; 66(20): 9837-44)
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Cites
DPC4 , A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1
Hahn, S. A., Schutte, M., Shamsul Hoque, A. T. M., Moskaluk, C. A., da Costa, L. T., Rozenblum, E., Weinstein, C. L., Fischer, A., Yeo, C. J., Hruban, R. H., et al. (1996) · Science · doi:10.1126/science.271.5247.350 · Cited by 2,337
TGF-β Signaling in Tumor Suppression and Cancer Progression
Derynck, R., Akhurst, R. J., & Balmain, A. (2001) · Nature Genetics · doi:10.1038/ng1001-117 · Cited by 2,275
TGF-ß Signaling in Fibroblasts Modulates the Oncogenic Potential of Adjacent Epithelia
Bhowmick, N. A., Chytil, A., Plieth, D., Gorska, A. E., Dumont, N., Shappell, S., Washington, M. K., Neilson, E. G., & Moses, H. L. (2004) · Science · doi:10.1126/science.1090922 · Cited by 1,401
Self-citationYang, L., DeBusk, L. M., Fukuda, K., Fingleton, B., Green-Jarvis, B., Shyr, Y., Matrisian, L. M., Carbone, D. P., & Lin, P. C. (2004) · Cancer Cell · doi:10.1016/j.ccr.2004.08.031 · Cited by 1,140
Zebrafish Prickle, a Modulator of Noncanonical Wnt/Fz Signaling, Regulates Gastrulation Movements
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Self-citationA targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors.
Fodde, R., Edelmann, W., Yang, K., van Leeuwen, C., Carlson, C., Renault, B., Breukel, C., Alt, E., Lipkin, M., & Khan, P. M. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.19.8969 · Cited by 531 · cited 1×
“5¶-TGGAAGGATTGGAGCTACGG-3¶, primer 3: 5¶-GTTGTCATCCAGGTCT-GGTG-3¶ that generate a 300 bp amplicon from the wild-type Apc allele and 400 bp amplicon from the Apc1638N mutant allele ( 25 ).”
Background
Cited by
Massagué, J. (2008) · Cell · doi:10.1016/j.cell.2008.07.001 · Cited by 3,907
Dependency of Colorectal Cancer on a TGF-β-Driven Program in Stromal Cells for Metastasis Initiation
Calon, A., Espinet, E., Palomo-Ponce, S., Tauriello, D. V. F., Iglesias, M., Céspedes, M. V., Sevillano, M., Nadal, C., Jung, P., Zhang, X. H.-F., et al. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.08.013 · Cited by 1,060
Yang, L., Huang, J., Ren, X., Gorska, A. E., Chytil, A., Aakre, M., Carbone, D. P., Matrisian, L. M., Richmond, A., Lin, P. C., et al. (2008) · Cancer Cell · doi:10.1016/j.ccr.2007.12.004 · Cited by 918
Self-citationTGF-β signaling in health and disease
Massagué, J., & Sheppard, D. (2023) · Cell · doi:10.1016/j.cell.2023.07.036 · Cited by 890
TGF-β Promotes Heterogeneity and Drug Resistance in Squamous Cell Carcinoma
Oshimori, N., Oristian, D., & Fuchs, E. (2015) · Cell · doi:10.1016/j.cell.2015.01.043 · Cited by 471
Metadata
- Authors
- Muñoz, N. M., Upton, M., Rojas, A., Washington, M. K., Lin, L., Chytil, A., Sozmen, E. G., Madison, B. B., Pozzi, A., Moon, R. T., Moses, H. L., & Grady, W. M.
- Venue
- Cancer Research
- Published
- 2006-10-15
- Volume
- 66
- Issue
- 20
- Pages
- 9837-9844
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2171262765
- Cited by
- 169
- References
- 6
- FWCI
- 4.91
- Type
- journal article
- Language
- en
- Open access
- closed
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- Muñoz, N. M., Upton, M., Rojas, A., Washington, M. K., Lin, L., Chytil, A., Sozmen, E. G., Madison, B. B., Pozzi, A., Moon, R. T., Moses, H. L., & Grady, W. M. (2006). Transforming Growth Factor β Receptor Type II Inactivation Induces the Malignant Transformation of Intestinal Neoplasms Initiated by Apc Mutation. Cancer Research. https://doi.org/10.1158/0008-5472.can-06-0890
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