Fandom

VroniPlag Wiki

Shg/Fragment 018 01

< Shg

31.380Seiten in
diesem Wiki
Seite hinzufügen
Diskussion0 Teilen

Störung durch Adblocker erkannt!


Wikia ist eine gebührenfreie Seite, die sich durch Werbung finanziert. Benutzer, die Adblocker einsetzen, haben eine modifizierte Ansicht der Seite.

Wikia ist nicht verfügbar, wenn du weitere Modifikationen in dem Adblocker-Programm gemacht hast. Wenn du sie entfernst, dann wird die Seite ohne Probleme geladen.


Typus
BauernOpfer
Bearbeiter
SleepyHollow02, Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 18, Zeilen: 1 ff. (entire page)
Quelle: Papadopoulou et al 2009
Seite(n): 57, 58, Zeilen: 57:right col., 6 ff., 58:figures 1, 2
Interestingly, while LNCaP prostate cancer cells express functional iAR, the DU145 cell line expresses either nonfunctional iAR, or is iAR-deficient. Therefore, DU145 cells fail to respond to iAR-regulated androgen treatment.[ Alimirah, F., et al 2006] In this cell model, mAR stimulation by testosterone or T-BSA conjugates induced potent actin reorganization, inhibited cell motility and promoted apoptotic regression. [Papadopoulou N, et al. 2008a] But the signaling pathway is different from LNCaP cells. Specifically, mAR activation bypassed the FAK/ PI-3K signaling pathway, as FAK was shown to be constitutively phosphorylated and mAR stimulation failed to further activate the downstream effectors PI-3K and Rac. An alternative pathway functionally distinct from the FAK/PI-3K/Rac signaling was described. [Papadopoulou N, et al. 2008a] This pathway regulated actin reorganization, the induction of apoptosis and the pro-apoptotic machinery. Indeed, long term down regulation of the pro-survival PI-3K/Akt pathway became evident 12–24 h upon mAR activation as indicated by the significant decrease of the phosphorylation levels of PI-3K and Akt. Furthermore, inhibition of NF-jkB translocation and increased FasL expression were documented, while increased caspase 3 activity was measured [Papadopoulou N, et al 2008b].

Shg 018ab diss.png

Figure 3: mAR signaling in human prostate cancer cells

A) Non-genomic mAR signaling operating in iAR positive LNCaP human prostate cancer cells regulating actin redistribution and apoptosis. Solid arrows indicate events that have been experimentally proven. Dashed arrows indicate unidentified possible links. See text for details.

B) Early and late mAR signaling operating in iAR deficient DU145 human prostate cancer cells regulating actin redistribution, downstream pro-apoptotic signaling, and migration. Solid arrows [indicate events that have been experimentally proven. Dashed arrows indicate unidentified possible links. See text for details. [Papadopoulou N, et al 2009]]


Alimirah, F., Chen, J., Basrawala, Z., Xin, H., and Choubey, D. (2006). DU-145 and PC-3 human prostate cancer cell lines express androgen receptor: implications for the androgen receptor functions and regulation. FEBS. Lett. 580, 2294–2300

Papadopoulou N, Charalampopoulos I, Alevizopoulos K, Gravanis A, Stournaras C. (2008 a). Rho/ROCK/Actin signaling regualtes membrane androgen receptor induced apoptosis in prostate cancer cells. Exp Cell Res, 314: 3162-3174.

Papadopoulou N, Charalampopoulos I, Anagnostopoulou V, Konstantinidis G, Föller M, Gravanis A, Alevizopoulos K, Lang F, Stournaras C. (2008 b). Membrane androgen receptor activation triggers down-regulation of PI-3K/Akt/NF-kappaB activity and induces apoptotic responses via Bad, FasL and caspase-3 in DU-145 prostate cancer cells. Mol Canc. 7:88.

[Page 57]

mAR Signaling in iAR-Deficient DU145 Prostate Cancer Cells

mAR expression was also reported in iAR-deficient DU145 prostate cancer cells (21). Interestingly, while LNCaP prostate cancer cells express functional intracellular androgen receptors (iAR), the DU145 cell line expresses either nonfunctional iAR (35), or is iAR-deficient (36, 37). Therefore, DU145 cells fail to respond to iAR-regulated androgen treatment (35). In this cell model, mAR stimulation by testosterone or T-BSA conjugates induced potent actin reorganization, inhibited cell motility and promoted apoptotic regression (21, 34). mAR signaling in DU145 cells was recently analyzed providing some very interesting results. Specifically, mAR activation bypassed the FAK/ PI-3K signaling pathway, as FAK was shown to be constitutively phosphorylated and mAR stimulation failed to further activate the downstream effectors PI-3K and Rac1. An alternative pathway functionally distinct from the FAK/PI-3K/Rac signaling was described. [...]. Functional analysis of the pathway revealed that Rho/ROCK signaling regulated, besides actin reorganization, the induction of apoptosis and the pro-apoptotic machinery. Indeed, long term down regulation of the pro-survival PI-3K/Akt pathway became evident 12–24 h upon mAR activation as indicated by the significant decrease of the phosphorylation levels of PI-3K and Akt. Furthermore, inhibition of NF-jB translocation and increased FasL expression were documented, while increased caspase 3 activity was measured (38).

[Page 58]

Shg 018a source.png

Figure 1. Non-genomic mAR signaling operating in iAR positive LNCaP human prostate cancer cells regulating actin redistribution and apoptosis. Solid arrows indicate events that have been experimentally proven. Dashed arrows indicate unidentified possible links. See text for details.

Shg 018b source.png

Figure 2. Early and late mAR signaling operating in iAR deficient DU145 human prostate cancer cells regulating actin redistribution, downstream pro-apoptotic signaling, and migration. Solid arrows indicate events that have been experimentally proven. Dashed arrows indicate unidentified possible links. See text for details.



21. Hatzoglou, A., Kampa, M., Kogia, C., Charalampopoulos, I., Theodoropoulos, P. A., Anezinis, P., Dambaki, C., Papakonstanti, E. A., Stathopoulos, E. A., Stournaras, C., Gravanis, A., and Castanas E. (2005) Membrane androgen receptor activation induces apoptotic regression of human prostate cancer cells in vitro and in vivo. J. Clin. Endocrinol. Metab. 90, 893–903.

34. Papadopoulou, N., Charalampopoulos, I., Alevizopoulos, K., Gravanis, A., and Stournaras, C. 2008. Rho/ROCK/Actin signaling regualtes membrane androgen receptor induced apoptosis in prostate cancer cells. Exp. Cell. Res., 314, 3162–3174.

35. Alimirah, F., Chen, J., Basrawala, Z., Xin, H., and Choubey, D. (2006) DU-145 and PC-3 human prostate cancer cell lines express androgen receptor: implications for the androgen receptor functions and regulation. FEBS. Lett. 580, 2294–2300.

36. Stone, K. R., Mickey, D. D., Wunderli, H., Mickey, G. H., and Paulson, D. F. (1978) Isolation of a human prostate carcinoma cell line (DU 145). Int. J. Cancer. 21, 274–281.

37. Mitchell, S., Abel, P., Ware, M., Stamp, G., and Lalani, E. (2000) Phenotypic and genotypic characterization of commonly used human prostatic cell lines. BJU. Int. 85, 932–944.

38. Papadopoulou, N., Charalampopoulos, I., Anagnostopoulou, V., Konstandinidis, G., Foeller, M., Gravanis, A., Alevizopoulos, K., Lang, F., and Stournaras, C. Membrane androgen receptor activation triggers down-regulation of PI-3K/AKT/NF-κB activity and induces apoptotic responses via Bad, FasL and caspase 3 in DU-145 prostate cancer cells, Submitted.

Anmerkungen

Although the source is given as reference for the figures, nothing has been marked as a citation.

Papadopoulou et al. (2008b) does not contain the copied text.

Sichter
(SleepyHollow02), (Graf Isolan), Hindemith

Auch bei Fandom

Zufälliges Wiki