The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Ionizing Radiation Enhances Matrix Metalloproteinase-2 Secretion and Invasion of Glioma Cells through Src/Epidermal Growth Factor Receptor–Mediated p38/Akt and Phosphatidylinositol 3-Kinase/Akt Signaling Pathways
Abstract
Glioblastoma is a severe type of primary brain tumor, and its highly invasive character is considered to be a major therapeutic obstacle. Several recent studies have reported that ionizing radiation (IR) enhances the invasion of tumor cells, but the mechanisms for this effect are not well understood. In this study, we investigated the possible signaling mechanisms involved in IR-induced invasion of glioma cells. IR increased the matrix metalloproteinase (MMP)-2 promoter activity, mRNA transcription, and protein secretion along with the invasiveness of glioma cells lacking functional PTEN (U87, U251, U373, and C6) but not those harboring wild-type (WT)-PTEN (LN18 and LN428). IR activated phosphatidylinositol 3-kinase (PI3K), Akt, and mammalian target of rapamycin, and blockade of these kinases by specific inhibitors (LY294002, Akt inhibitor IV, and rapamycin, respectively) and transfection of dominant-negative (DN) mutants (DN-p85 and DN-Akt) or WT-PTEN suppressed the IR-induced MMP-2 secretion in U251 and U373 cells. In addition, inhibitors of epidermal growth factor receptor (EGFR; AG490 and AG1478), Src (PP2), and p38 (SB203580), EGFR neutralizing antibody, and transfection of DN-Src and DN-p38 significantly blocked IR-induced Akt phosphorylation and MMP-2 secretion. IR-induced activation of EGFR was suppressed by PP2, whereas LY294002 and SB203580 did not affect the activations of p38 and PI3K, respectively. Finally, these kinase inhibitors significantly reduced the IR-induced invasiveness of these cells on Matrigel. Taken together, our findings suggest that IR induces Src-dependent EGFR activation, which triggers the p38/Akt and PI3K/Akt signaling pathways, leading to increased MMP-2 expression and heightened invasiveness of PTEN mutant glioma cells. (Cancer Res 2006; 66(17): 8511-9)
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1 retracted
Koul, D., Parthasarathy, R. V., Shen, R., Davies, M. A., Jasser, S. A., Chintala, S. K., Rao, J. S., Sun, Y., Benvenisite, E. N., Liu, T.-J., et al. (2001) · Oncogene · doi:10.1038/sj.onc.1204799 · Cited by 115
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Inhibition of cell migration, spreading, and focal adhesions by tumor suppressor PTEN
Tamura, M., Gu, J., Matsumoto, K., Aota, S.-I., Parsons, R., & Yamada, K. M. (1998) · Science · doi:10.1126/science.280.5369.1614 · Cited by 1,215
Cost of Migration: Invasion of Malignant Gliomas and Implications for Treatment
Giese, A., Bjerkvig, R., Berens, M. E., & Westphal, M. (2003) · Journal of Clinical Oncology · doi:10.1200/jco.2003.05.063 · Cited by 1,200
The lipid phosphatase activity of PTEN is critical for its tumor supressor function
Myers, M. P., Pass, I., Batty, I. H., Van der Kaay, J., Stolarov, J. P., Hemmings, B. A., Wigler, M. H., Downes, C. P., & Tonks, N. K. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.23.13513 · Cited by 1,168
Molecular mechanisms of glioma invasiveness: the role of proteases
Rao, J. S. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1121 · Cited by 847
Gelatinase-mediated migration and invasion of cancer cells
Björklund, M., & Koivunen, E. (2005) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2005.03.001 · Cited by 661
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Wild‐Bode, C., Weller, M., Rimner, A., DICHGANS, J., & Wick, W. (2001) · PubMed · Cited by 464
Stress and Radiation-Induced Activation of Multiple Intracellular Signaling Pathways1
Dent, P., Yacoub, A., Contessa, J., Caron, R., Amorino, G., Valerie, K., Hagan, M. P., Grant, S., & Schmidt-Ullrich, R. (2003) · Radiation Research · doi:10.1667/0033-7587(2003)159[0283:sariao]2.0.co;2 · Cited by 463
Cited by
Roy, S., Khanna, S., Hussain, S.-R. A., Biswas, S., Azad, A., Rink, C., Gnyawali, S., Shilo, S., Nuovo, G. J., & Sen, C. K. (2009) · Cardiovascular Research · doi:10.1093/cvr/cvp015 · Cited by 614
Lee, S. Y., Jeong, E. K., Ju, M. K., Jeon, H. M., Kim, M. Y., Kim, C. H., Park, H. G., Han, S. I., & Kang, H. S. (2017) · Molecular Cancer · doi:10.1186/s12943-016-0577-4 · Cited by 578
Self-citationZhou, X., Ren, Y., Moore, L., Mei, M., You, Y., Xu, P., Wang, B., Wang, G., Jia, Z., Pu, P., et al. (2010) · Laboratory Investigation · doi:10.1038/labinvest.2009.126 · Cited by 358
Yes and PI3K Bind CD95 to Signal Invasion of Glioblastoma
Kleber, S., Sancho-Martinez, I., Wiestler, B., Beisel, A., Gieffers, C., Hill, O., Thiemann, M., Mueller, W., Sykora, J., Kuhn, A., et al. (2008) · Cancer Cell · doi:10.1016/j.ccr.2008.02.003 · Cited by 309
Inhibition of MMP 14 potentiates the therapeutic effect of temozolomide and radiation in gliomas
Ulasov, I., Thaci, B., Sarvaiya, P., Yi, R., Guo, D., Auffinger, B., Pytel, P., Zhang, L., Kim, C. K., Borovjagin, A., et al. (2013) · Cancer Medicine · doi:10.1002/cam4.104 · Cited by 28
Metadata
- Authors
- Park, C.-M., Park, M.-J., Kwak, H.-J., Lee, H.-C., Kim, M.-S., Lee, S.-H., Park, I.-C., Rhee, C. H., & Hong, S.-I.
- Venue
- Cancer Research
- Published
- 2006-09-01
- Volume
- 66
- Issue
- 17
- Pages
- 8511-8519
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2003736915
- Cited by
- 282
- References
- 39
- FWCI
- 5.39
- Type
- journal article
- Language
- en
- Open access
- closed
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- Park, C.-M., Park, M.-J., Kwak, H.-J., Lee, H.-C., Kim, M.-S., Lee, S.-H., Park, I.-C., Rhee, C. H., & Hong, S.-I. (2006). Ionizing Radiation Enhances Matrix Metalloproteinase-2 Secretion and Invasion of Glioma Cells through Src/Epidermal Growth Factor Receptor–Mediated p38/Akt and Phosphatidylinositol 3-Kinase/Akt Signaling Pathways. Cancer Research. https://doi.org/10.1158/0008-5472.can-05-4340
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