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Cited by 524

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

AKT-Independent Signaling Downstream of Oncogenic PIK3CA Mutations in Human Cancer

Open access
Vasudevan, Krishna M., Barbie, David A., Davies, Michael A., Rabinovsky, Rosalia, McNear, Chontelle J., Kim, Jessica J., Hennessy, Bryan T., Tseng, Hsiuyi, Pochanard, Panisa, Kim, So Young, Dunn, Ian F., Schinzel, Anna C., Sandy, Peter, Hoersch, Sebastian, Sheng, Qing, Gupta, Piyush B., Boehm, Jesse S., Reiling, Jan H., Silver, Serena, Lu, Yiling, Stemke-Hale, Katherine, Dutta, Bhaskar, Joy, Corwin, Sahin, Aysegul A., Gonzalez-Angulo, Ana Maria, Lluch, Ana, Rameh, Lucia E., Jacks, Tyler, Root, David E., Lander, Eric S., Mills, Gordon B., Hahn, William C., Sellers, William R., Garraway, Levi A.·2009·Cancer Cell
DOI 10.1016/j.ccr.2009.04.012
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Abstract

Summary Dysregulation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway occurs commonly in human cancer. PTEN tumor suppressor or PIK3CA oncogene mutations both direct PI3K-dependent tumorigenesis largely through activation of the AKT/PKB kinase. However, here we show through phospho-protein profiling and functional genomic studies that many PIK3CA-mutant cancer cell lines and human breast tumors exhibit only minimal AKT activation, and a diminished reliance on AKT for anchorage-independent growth. Instead, these cells retain robust PDK1 activation and membrane localization, and exhibit dependency on the PDK1 substrate SGK3. SGK3 undergoes PI3K- and PDK1-dependent activation in PIK3CA-mutant cancer cells. Thus, PI3K may promote cancer through both AKT-dependent and AKT-independent mechanisms. Knowledge of differential PI3K/PDK1 signaling could inform rational therapeutics in cancers harboring PIK3CA mutations.

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Authors
Vasudevan, K. M., Barbie, D. A., Davies, M. A., Rabinovsky, R., McNear, C. J., Kim, J. J., Hennessy, B. T., Tseng, H., Pochanard, P., Kim, S. Y., Dunn, I. F., Schinzel, A. C., Sandy, P., Hoersch, S., Sheng, Q., Gupta, P. B., Boehm, J. S., Reiling, J. H., Silver, S., Lu, Y., Stemke-Hale, K., Dutta, B., Joy, C., Sahin, A. A., Gonzalez-Angulo, A. M., Lluch, A., Rameh, L. E., Jacks, T., Root, D. E., Lander, E. S., Mills, G. B., Hahn, W. C., Sellers, W. R., & Garraway, L. A.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2009-07
Volume
16
Issue
1
Pages
21-32
ISSN
1535-6108 (ISSN-L)
DOI
10.1016/j.ccr.2009.04.012
OpenAlex
W1588880778
Cited by
524
References
5
FWCI
17.64
Type
journal article
Language
en
Open access
bronze

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