The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Akt/PKB promotes cancer cell invasion via increased motility and metalloproteinase production
Abstract
The Akt/protein kinase B (PKB) serine/ threonine kinase is well known as an important mediator of many cell survival signaling pathways. Here, we demonstrate for the first time a major role of Akt/PKB in the cell invasion properties of the highly metastatic cell line HT1080. Using confocal microscopic analyses of live samples, we found Akt/PKB to be localized in the leading edge membrane area of migrating HT1080 cells. This localization was dependent on phosphoino‐sitide 3‐kinase and required the lipid binding ability of the phosphoinositide binding pleckstrin homology domain of Akt/PKB. We examined the possible function of Akt/PKB in HT1080 invasion. Surprisingly, Akt/ PKB potently promoted HT1080 invasion, by increasing cell motility and matrix metalloproteinase‐9 (MMP‐9) production, in a manner highly dependent on its kinase activity and membrane‐translocating ability. The increase in MMP‐9 production was mediated by activation of nuclear factor‐κB transcriptional activity by Akt/PKB. However, Akt/PKB did not affect the cell‐cell or cell‐matrix adhesion properties of HT1080. Our findings thus establish Akt/PKB as a major factor in the invasive abilities of cancer cells.
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Cites
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Cited by
Mutant PIK3CA promotes cell growth and invasion of human cancer cells.
Samuels, Y., Diaz, L. A., Schmidt-Kittler, O., Cummins, J. M., DeLong, L., Cheong, I., Rago, C., Huso, D. L., Lengauer, C., Kinzler, K. W., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.05.014 · Cited by 915
RAS Interaction with PI3K: More Than Just Another Effector Pathway
Castellano, E., & Downward, J. (2011) · Genes & Cancer · doi:10.1177/1947601911408079 · Cited by 762
Endothelial to Mesenchymal Transition in Cardiovascular Disease
Kovacic, J. C., Dimmeler, S., Harvey, R. P., Finkel, T., Aikawa, E., Krenning, G., & Baker, A. H. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.09.089 · Cited by 631
Miao, H., Li, D.-Q., Mukherjee, A., Guo, H., Petty, A., Cutter, J., Basilion, J. P., Sedor, J., Wu, J., Danielpour, D., et al. (2009) · Cancer Cell · doi:10.1016/j.ccr.2009.04.009 · Cited by 533
Akt inhibition promotes autophagy and sensitizes PTEN-null tumors to lysosomotropic agents
Degtyarev, M., De Mazière, A., Orr, C., Lin, J., Lee, B. B., Tien, J. Y., Prior, W. W., van Dijk, S., Wu, H., Gray, D. C., et al. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200801099 · Cited by 366
Metadata
- Authors
- DOHOON, K., SUNHONG, K., HYONGJONG, K., SANG‐OH, Y., AN‐SIK, C., KYOUNG SANG, C., & JONGKYEONG, C.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2001-09
- Volume
- 15
- Issue
- 11
- Pages
- 1953-1962
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2071531606
- Cited by
- 489
- References
- 45
- FWCI
- 5.97
- Type
- journal article
- Language
- en
- Open access
- closed
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- DOHOON, K., SUNHONG, K., HYONGJONG, K., SANG‐OH, Y., AN‐SIK, C., KYOUNG SANG, C., & JONGKYEONG, C. (2001). Akt/PKB promotes cancer cell invasion via increased motility and metalloproteinase production. The FASEB Journal. https://doi.org/10.1096/fj.01-0198com
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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