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Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 31, Zeilen: 10-32
Quelle: Manning und Cantley 2007
Seite(n): 1269, Zeilen: li.Sp.43 ff. - re.Sp. 1-17
A role for Akt in the control of cell migration, invasion of the extracellular matrix, and ultimately metastasis has been difficult to ascertain. Strikingly, activation of Akt1 has been found to decrease mammary epithelial cell migration, and Akt1 prevents an epithelial-to-mesenchymal transition that resembles events required for metastasis [Irie et al., 2005] and [Yoeli-Lerner et al., 2005]. Two independent mechanisms for this surprising Akt function have been explored. The first found that the inhibitory effect of Akt1 on the in vitro migration and invasion properties of breast cancer cell lines involved a pathway leading to degradation of the nuclear factor of activated T cells (NFAT) transcription factors [Yoeli-Lerner et al., 2005]. However, the molecular mechanism of Akt1-mediated degradation of NFAT is currently unknown. A second group found that siRNA knockdown of Akt1, but not Akt2, led to an increase in the migration of mammary epithelial cells [Irie et al., 2005]. Loss of Akt1, specifically, led to an increase in the activation of Erk1 and Erk2, which was found to be required for the enhanced migration. Again, the mechanism by which Akt1, but not Akt2, inhibits Erk signaling in this system remains unknown. Interestingly, mouse tumor models have also suggested that Akt1 inhibits metastases [Hutchinson et al., 2004], whereas Akt2 promotes metastases [Arboleda et al., 2003]. However, these differential effects of Akt1 and Akt2 on epithelial cell migration may not translate to other cell types. In fact, studies on cell migration using mouse embryonic fibroblasts deficient of specific Akt isoforms have suggested opposite effects on fibroblast migration, with Akt1 promoting migration and with Akt2 inhibiting it [ [Zhou et al., 2006].]

G.L. Zhou, D.F. Tucker, S.S. Bae, K. Bhatheja, M.J. Birnbaum and J. Field. (2006). Opposing roles for Akt1 and Akt2 in Rac/Pak signaling and cell migration, J. Biol. Chem. 281 ,pp. 36443–36453.

Hutchinson, J. Jin, R.D. Cardiff, J.R. Woodgett and W.J. Muller. (2004). Activation of Akt-1 (PKB-alpha) can accelerate ErbB-2-mediated mammary tumorigenesis but suppresses tumor invasion, Cancer Res. 64 (2004), pp. 3171–3178.

M.J. Arboleda, J.F. Lyons, F.F. Kabbinavar, M.R. Bray, B.E. Snow, R. Ayala, M. Danino, B.Y. Karlan and D.J. Slamon,. (2003). Overexpression of AKT2/protein kinase Bbeta leads to up-regulation of beta1 integrins, increased invasion, and metastasis of human breast and ovarian cancer cells, Cancer Res. 63 pp. 196–206.

Yoeli-Lerner, G.K. Yiu, I. Rabinovitz, P. Erhardt, S. Jauliac and A. Toker. (2005). Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT, Mol. Cell 20, pp. 539–550.

Cell Migration and Invasion

Until recently, a role for Akt in the control of cell migration, invasion of the extracellular matrix, and ultimately metastasis has been difficult to ascertain. Strikingly, activation of Akt1 has been found to decrease mammary epithelial cell migration, and Akt1 prevents an epithelial-to-mesenchymal transition that resembles events required for metastasis (Irie et al., 2005; Yoeli-Lerner et al., 2005). Two independent mechanisms for this surprising Akt function have been explored. The first found that the inhibitory effect of Akt1 on the in vitro migration and invasion properties of breast cancer cell lines involved a pathway leading to degradation of the nuclear factor of activated T cells (NFAT) transcription factors (Yoeli-Lerner et al., 2005). However, the molecular mechanism of Akt1-mediated degradation of NFAT is currently unknown. A second group found that siRNA knockdown of Akt1, but not Akt2, led to an increase in the migration of mammary epithelial cells (Irie et al., 2005). Loss of Akt1, specifically, led to an increase in the activation of Erk1 and Erk2, which was found to be required for the enhanced migration. Again, the mechanism by which Akt1, but not Akt2, inhibits Erk signaling in this system remains unknown. Interestingly, mouse tumor models have also suggested that Akt1 inhibits metastases (Hutchinson et al., 2004), whereas Akt2 promotes metastases (Arboleda et al., 2003). However, these differential effects of Akt1 and Akt2 on epithelial cell migration may not translate to other cell types. In fact, studies on cell migration using mouse embryonic fibroblasts deficient of specific Akt isoforms have suggested opposite effects on fibroblast migration, with Akt1 promoting migration and with Akt2 inhibiting it (Zhou et al., 2006).


Arboleda, M.J., Lyons, J.F., Kabbinavar, F.F., Bray, M.R., Snow, B.E., Ayala, R., Danino, M., Karlan, B.Y., and Slamon, D.J. (2003). Overexpression of AKT2/protein kinase Bbeta leads to up-regulation of beta1 integrins, increased invasion, and metastasis of human breast and ovarian cancer cells. Cancer Res. 63, 196–206.

Hutchinson, J.N., Jin, J., Cardiff, R.D., Woodgett, J.R., and Muller, W.J. (2004). Activation of Akt-1 (PKB-alpha) can accelerate ErbB-2- mediated mammary tumorigenesis but suppresses tumor invasion. Cancer Res. 64, 3171–3178.

Irie, H.Y., Pearline, R.V., Grueneberg, D., Hsia, M., Ravichandran, P., Kothari, N., Natesan, S., and Brugge, J.S. (2005). Distinct roles of Akt1 and Akt2 in regulating cell migration and epithelial-mesenchymal transition. J. Cell Biol. 171, 1023–1034.

Yoeli-Lerner, M., Yiu, G.K., Rabinovitz, I., Erhardt, P., Jauliac, S., and Toker, A. (2005). Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT. Mol. Cell 20, 539–550.

Zhou, G.L., Tucker, D.F., Bae, S.S., Bhatheja, K., Birnbaum, M.J., and Field, J. (2006). Opposing roles for Akt1 and Akt2 in Rac/Pak signaling and cell migration. J. Biol. Chem. 281, 36443–36453.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Eine Referenz für [Irie et al., 2005] fehlt im Literaturverzeichnis von Shg.

Sichter
(Graf Isolan), SleepyHollow02

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