AKT Status Controls Susceptibility of Malignant Keratinocytes to the Early-Activated and UVB-Induced Apoptotic Pathway David Decraene, An Van Laethem,

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Presentation transcript:

AKT Status Controls Susceptibility of Malignant Keratinocytes to the Early-Activated and UVB-Induced Apoptotic Pathway David Decraene, An Van Laethem, Patrizia Agostinis, Lucie De Peuter, Hugo Degreef, Roger Bouillon, Marjan Garmyn Journal of Investigative Dermatology Volume 123, Issue 1, Pages 207-212 (July 2004) DOI: 10.1111/j.0022-202X.2004.22702.x Copyright © 2004 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 Basal p53 and AKT protein levels in normal human keratinocytes (NHK), A253, and A431 cells. Primary human keratinocytes (NHK), A253 cells (A253 p53(-)), A253 cells stably re-expressing wild type p53 (A253 p53(+)) and A431 cells (A431) were lysed and subjected to an SDS-PAGE. p53 and AKT proteins levels were analyzed by immunoblotting with anti-p53 and anti-AKT antiserum as described under “Materials and Methods”. Journal of Investigative Dermatology 2004 123, 207-212DOI: (10.1111/j.0022-202X.2004.22702.x) Copyright © 2004 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 Growth factor-deprived A431 cells are sensitized to the early-activated and ultraviolet B (UVB)-induced apoptotic pathway. A431 cells were cultured in growth factor-deprived medium as described in “Materials and Methods”. (A) Western blot analysis of the time course for caspase-3-induced poly(ADP-ribose)polymerase (PARP) cleavage in UVB-irradiated (100 mJ per cm2) A431 cells. Lysates were collected at the indicated time points. (B) (a–c) Microscopic images of cells stained with Hoechst dye, taken 5 h after irradiation with 100 mJ per cm2 UVB (arrows indicate cells with condensed chromatin). (d–f) Cell cycle analysis of A431 cells, 5 h after irradiation with 100 mJ per cm2 UVB. Growth factor-deprived A431 cells were sham-irradiated (a, d), UVB-irradiated (b, e), or supplemented with insulin-like growth factor-1 (IGF-1) and UVB-irradiated (c, f). In all of the above experiments, IGF-1 (10 ng per mL) was added 30 min before UVB-irradiation. Journal of Investigative Dermatology 2004 123, 207-212DOI: (10.1111/j.0022-202X.2004.22702.x) Copyright © 2004 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 3 Growth factor-deprived A253 cells are completely resistant to the early-activated and ultraviolet B (UVB)-induced apoptotic pathway, in a wortmannin-sensitive fashion. A253 cells were cultured in growth factor-deprived medium as described in “Materials and Methods”. (A) Western blot analysis of the time course for caspase-3-induced poly(ADP-ribose)polymerase (PARP) cleavage in UVB-irradiated (100 mJ per cm2) A253 cells lacking endogenous p53-expression (A253-p53(-)) and cells stably re-expressing wild-type (wt)-p53 (A253-p53(+)). Cell lysates were collected at the indicated time points. (B) A253 cells (stably re-expressing wt-p53 were indicated) were pre-treated with 1 μM wortmannin for 1 h and subsequently exposed to 100 mJ per cm2 UVB. Cell lysates were collected at the indicated time points. PARP cleavage was analyzed by western blotting as described. (C) (a–d) Microscopic images of cells stained with Hoechst dye, taken 5 h after irradiation with 100 mJ per cm2 UVB (arrows indicate cells with condensed chromatin). (e–h) Cell cycle analysis of growth factor-deprived A253 cells, 5 h after irradiation with 100 mJ per cm2 UVB. (a, e) A253-p53(-) cells, (b, f) A253-p53(-) cells pre-treated with 1 μM wortmannin, (c, g) A253-p53(+) cells, (d, h) A253-p53(+) cells pre-treated with 1 μM wortmannin. Journal of Investigative Dermatology 2004 123, 207-212DOI: (10.1111/j.0022-202X.2004.22702.x) Copyright © 2004 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 4 Sensitivity of squamous cell carcinoma cell lines to the early-activated and ultraviolet B (UVB)-induced apoptotic pathway correlates with the AKT phosphorylation status. Cells were cultured in growth factor-deprived medium as described under “Materials and Methods”. (A) AKT phosphorylation status was evaluated by western blotting. Following a 15 min incubation in the absence or in the presence of insulin-like growth factor-1 (IGF-1) (10 ng per mL), cell lysates were collected. Proteins were separated by SDS-PAGE and analyzed by immunoblotting as described in “Materials and Methods”. NHK, normal human keratinocytes; A253-p53(-), A253 cells that lack endogenous p53 expression; A253-p53(+), A253 cells stably re-expressing wild-type (wt)-p53. (B) A253 cells lacking endogenous p53 expression (-) and A253 cells stably re-expressing wt-p53 (+) were treated with Wortmannin (1 μM) and scraped at the indicated time point. AKT phosphorylation status was evaluated by immunoblotting with phospho-specific antibodies as described under “Materials and Methods”. Journal of Investigative Dermatology 2004 123, 207-212DOI: (10.1111/j.0022-202X.2004.22702.x) Copyright © 2004 The Society for Investigative Dermatology, Inc Terms and Conditions