The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML
Open accessAbstract
The mTOR complex 2 (mTORC2) containing mTOR and rictor is thought to be rapamycin insensitive and was recently shown to regulate the prosurvival kinase AKT by phosphorylation on Ser473. We investigated the molecular effects of mTOR inhibition by the rapamycin derivatives (RDs) temsirolimus (CCI-779) and everolimus (RAD001) in acute myeloid leukemia (AML) cells. Unexpectedly, RDs not only inhibited the mTOR complex 1 (mTORC1) containing mTOR and raptor with decreased p70S6K, 4EPB1 phosphorylation, and GLUT1 mRNA, but also blocked AKT activation via inhibition of mTORC2 formation. This resulted in suppression of phosphorylation of the direct AKT substrate FKHR and decreased transcription of D-cyclins in AML cells. Similar observations were made in samples from patients with hematologic malignancies who received RDs in clinical studies. Our study provides the first evidence that rapamycin derivatives inhibit AKT signaling in primary AML cells both in vitro and in vivo, and supports the therapeutic potential of mTOR inhibition strategies in leukemias.
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Cites
Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex
Sarbassov, D. D., Guertin, D. A., Ali, S. M., & Sabatini, D. M. (2005) · Science · doi:10.1126/science.1106148 · Cited by 6,216
Self-citationTOR signaling in growth and metabolism
Wullschleger, S., Loewith, R., & Hall, M. N. (2006) · Cell · doi:10.1016/j.cell.2006.01.016 · Cited by 5,787
mTOR Inhibition Induces Upstream Receptor Tyrosine Kinase Signaling and Activates Akt
O'Reilly, K. E., Rojo, F., She, Q.-B., Solit, D., Mills, G. B., Smith, D., Lane, H., Hofmann, F., Hicklin, D. J., Ludwig, D. L., et al. (2006) · Cancer Research · doi:10.1158/0008-5472.can-05-2925 · Cited by 2,561
Prolonged Rapamycin Treatment Inhibits mTORC2 Assembly and Akt/PKB
Sarbassov, D. D., Ali, S. M., Sengupta, S., Sheen, J.-H., Hsu, P. P., Bagley, A. F., Markhard, A. L., & Sabatini, D. M. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.03.029 · Cited by 2,365
Self-citationRaptor, a Binding Partner of Target of Rapamycin (TOR), Mediates TOR Action
Hara, K., Maruki, Y., Long, X., Yoshino, K.-I., Oshiro, N., Hidayat, S., Tokunaga, C., Avruch, J., & Yonezawa, K. (2002) · Cell · doi:10.1016/s0092-8674(02)00833-4 · Cited by 1,810
The tor pathway: a target for cancer therapy
Bjornsti, M.-A., & Houghton, P. J. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1362 · Cited by 1,314
Majumder, P. K., Febbo, P. G., Bikoff, R., Berger, R., Xue, Q., McMahon, L. M., Manola, J., Brugarolas, J., McDonnell, T. J., Golub, T. R., et al. (2004) · Nature Medicine · doi:10.1038/nm1052 · Cited by 964
A novel mechanism of gene regulation and tumor suppression by the transcription factor FKHR
Ramaswamy, S., Nakamura, N., Sansal, I., Bergeron, L., & Sellers, W. R. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00086-7 · Cited by 428
Yee, K. W. L., Zeng, Z., Konopleva, M., Verstovsek, S., Ravandi, F., Ferrajoli, A., Thomas, D., Wierda, W., Apostolidou, E., Albitar, M., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-0764 · Cited by 285
Self-citationMammalian target of rapamycin inhibition as therapy for hematologic malignancies
Panwalkar, A., Verstovsek, S., & Giles, F. J. (2004) · Cancer · doi:10.1002/cncr.20026 · Cited by 208
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Cited by
Defining the role of mTOR in cancer
Guertin, D. A., & Sabatini, D. M. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.05.008 · Cited by 2,833
Self-citationSpilman, P., Podlutskaya, N., Hart, M. J., Debnath, J., Gorostiza, O., Bredesen, D., Richardson, A., Strong, R., & Galvan, V. (2010) · PLoS ONE · doi:10.1371/journal.pone.0009979 · Cited by 1,033
“Active mTORC2 phosphorylates and activates Akt and PKC[15,16].”
BackgroundPanwar, V., Singh, A., Bhatt, M., Tonk, R. K., Azizov, S., Raza, A. S., Sengupta, S., Kumar, D., & Garg, M. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01608-z · Cited by 967
The mTOR Signalling Pathway in Human Cancer
Pópulo, H., Lopes, J. M., & Soares, P. (2012) · International Journal of Molecular Sciences · doi:10.3390/ijms13021886 · Cited by 830
Bhaskar, P. T., & Hay, N. (2007) · Developmental Cell · doi:10.1016/j.devcel.2007.03.020 · Cited by 798
Metadata
- Authors
- Zeng, Z., Sarbassov, D. D., Samudio, I. J., Yee, K. W. L., Munsell, M. F., Ellen Jackson, C., Giles, F. J., Sabatini, D. M., Andreeff, M., & Konopleva, M.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2006-12-19
- Volume
- 109
- Issue
- 8
- Pages
- 3509-3512
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1970550717
- Cited by
- 342
- References
- 14
- FWCI
- 10.44
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Zeng, Z., Sarbassov, D. D., Samudio, I. J., Yee, K. W. L., Munsell, M. F., Ellen Jackson, C., Giles, F. J., Sabatini, D. M., Andreeff, M., & Konopleva, M. (2007). Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML. Blood. https://doi.org/10.1182/blood-2006-06-030833
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