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Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation
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| Zeitschriftentitel: | International Journal of Cancer |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | International Journal of Cancer, 129, 2011, 8, S. 2025-2031 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Akakura, Shin Bouchard, Rene Bshara, Wiam Morrison, Carl Gelman, Irwin H. Akakura, Shin Bouchard, Rene Bshara, Wiam Morrison, Carl Gelman, Irwin H. |
|---|---|
| author |
Akakura, Shin Bouchard, Rene Bshara, Wiam Morrison, Carl Gelman, Irwin H. |
| spellingShingle |
Akakura, Shin Bouchard, Rene Bshara, Wiam Morrison, Carl Gelman, Irwin H. International Journal of Cancer Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation Cancer Research Oncology |
| author_sort |
akakura, shin |
| spelling |
Akakura, Shin Bouchard, Rene Bshara, Wiam Morrison, Carl Gelman, Irwin H. 0020-7136 1097-0215 Wiley Cancer Research Oncology http://dx.doi.org/10.1002/ijc.25828 <jats:title>Abstract</jats:title><jats:p>The ability of SSeCKS/Gravin/AKAP12 (SSeCKS) to negatively regulate cell cycle progression is thought to relate to its spatiotemporal scaffolding activity for key signaling molecules such as protein kinase A and C, calmodulin and cyclins. SSeCKS is downregulated upon progression to malignancy in many cancer types, including melanoma and nonmelanoma skin cancer. The forced re‐expression of SSeCKS is especially potent in suppressing metastasis through the inhibition of VEGF‐mediated neovascularization. We have previously shown that SSeCKS‐null (KO) mice exhibit hyperplasia and focal dysplasia in the prostate marked by activated Akt. To address whether KO mice exhibit increased skin carcinogenesis, WT and KO C57BL/6 mice were treated topically with 12‐<jats:italic>O</jats:italic>‐tetradecanoylphorbol‐13‐acetate and 7,12‐dimethylbenzanthracene. Compared to WT mice, KO mice developed squamous papillomas more rapidly and in greater numbers and also exhibited significantly increased progression to squamous cell carcinoma. Untreated KO epidermal layers were thicker than those in age‐matched WT mice and exhibited significantly increased levels of FAK and phospho‐ERK1/2, known mediators of carcinogen‐induced squamous papilloma progression to carcinoma. Compared to protein levels in WT mouse embryo fibroblasts (MEF), SSeCKS levels were increased in FAK‐null cells, whereas FAK levels were increased in SSeCKS‐null cells. RNAi studies in WT MEF cells suggest that SSeCKS and FAK attenuate each other's expression. Our study implicates a role for SSeCKS in preventing of skin cancer progression possibly through negatively regulating FAK expression.</jats:p> Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation International Journal of Cancer |
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Wiley, 2011 |
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0020-7136 1097-0215 |
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| title |
Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_unstemmed |
Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_full |
Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_fullStr |
Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_full_unstemmed |
Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_short |
Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_sort |
carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the ssecks/akap12 metastasis suppressor correlate with fak upregulation |
| topic |
Cancer Research Oncology |
| url |
http://dx.doi.org/10.1002/ijc.25828 |
| publishDate |
2011 |
| physical |
2025-2031 |
| description |
<jats:title>Abstract</jats:title><jats:p>The ability of SSeCKS/Gravin/AKAP12 (SSeCKS) to negatively regulate cell cycle progression is thought to relate to its spatiotemporal scaffolding activity for key signaling molecules such as protein kinase A and C, calmodulin and cyclins. SSeCKS is downregulated upon progression to malignancy in many cancer types, including melanoma and nonmelanoma skin cancer. The forced re‐expression of SSeCKS is especially potent in suppressing metastasis through the inhibition of VEGF‐mediated neovascularization. We have previously shown that SSeCKS‐null (KO) mice exhibit hyperplasia and focal dysplasia in the prostate marked by activated Akt. To address whether KO mice exhibit increased skin carcinogenesis, WT and KO C57BL/6 mice were treated topically with 12‐<jats:italic>O</jats:italic>‐tetradecanoylphorbol‐13‐acetate and 7,12‐dimethylbenzanthracene. Compared to WT mice, KO mice developed squamous papillomas more rapidly and in greater numbers and also exhibited significantly increased progression to squamous cell carcinoma. Untreated KO epidermal layers were thicker than those in age‐matched WT mice and exhibited significantly increased levels of FAK and phospho‐ERK1/2, known mediators of carcinogen‐induced squamous papilloma progression to carcinoma. Compared to protein levels in WT mouse embryo fibroblasts (MEF), SSeCKS levels were increased in FAK‐null cells, whereas FAK levels were increased in SSeCKS‐null cells. RNAi studies in WT MEF cells suggest that SSeCKS and FAK attenuate each other's expression. Our study implicates a role for SSeCKS in preventing of skin cancer progression possibly through negatively regulating FAK expression.</jats:p> |
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| author | Akakura, Shin, Bouchard, Rene, Bshara, Wiam, Morrison, Carl, Gelman, Irwin H. |
| author_facet | Akakura, Shin, Bouchard, Rene, Bshara, Wiam, Morrison, Carl, Gelman, Irwin H., Akakura, Shin, Bouchard, Rene, Bshara, Wiam, Morrison, Carl, Gelman, Irwin H. |
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| description | <jats:title>Abstract</jats:title><jats:p>The ability of SSeCKS/Gravin/AKAP12 (SSeCKS) to negatively regulate cell cycle progression is thought to relate to its spatiotemporal scaffolding activity for key signaling molecules such as protein kinase A and C, calmodulin and cyclins. SSeCKS is downregulated upon progression to malignancy in many cancer types, including melanoma and nonmelanoma skin cancer. The forced re‐expression of SSeCKS is especially potent in suppressing metastasis through the inhibition of VEGF‐mediated neovascularization. We have previously shown that SSeCKS‐null (KO) mice exhibit hyperplasia and focal dysplasia in the prostate marked by activated Akt. To address whether KO mice exhibit increased skin carcinogenesis, WT and KO C57BL/6 mice were treated topically with 12‐<jats:italic>O</jats:italic>‐tetradecanoylphorbol‐13‐acetate and 7,12‐dimethylbenzanthracene. Compared to WT mice, KO mice developed squamous papillomas more rapidly and in greater numbers and also exhibited significantly increased progression to squamous cell carcinoma. Untreated KO epidermal layers were thicker than those in age‐matched WT mice and exhibited significantly increased levels of FAK and phospho‐ERK1/2, known mediators of carcinogen‐induced squamous papilloma progression to carcinoma. Compared to protein levels in WT mouse embryo fibroblasts (MEF), SSeCKS levels were increased in FAK‐null cells, whereas FAK levels were increased in SSeCKS‐null cells. RNAi studies in WT MEF cells suggest that SSeCKS and FAK attenuate each other's expression. Our study implicates a role for SSeCKS in preventing of skin cancer progression possibly through negatively regulating FAK expression.</jats:p> |
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| imprint | Wiley, 2011 |
| imprint_str_mv | Wiley, 2011 |
| institution | DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1 |
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| spelling | Akakura, Shin Bouchard, Rene Bshara, Wiam Morrison, Carl Gelman, Irwin H. 0020-7136 1097-0215 Wiley Cancer Research Oncology http://dx.doi.org/10.1002/ijc.25828 <jats:title>Abstract</jats:title><jats:p>The ability of SSeCKS/Gravin/AKAP12 (SSeCKS) to negatively regulate cell cycle progression is thought to relate to its spatiotemporal scaffolding activity for key signaling molecules such as protein kinase A and C, calmodulin and cyclins. SSeCKS is downregulated upon progression to malignancy in many cancer types, including melanoma and nonmelanoma skin cancer. The forced re‐expression of SSeCKS is especially potent in suppressing metastasis through the inhibition of VEGF‐mediated neovascularization. We have previously shown that SSeCKS‐null (KO) mice exhibit hyperplasia and focal dysplasia in the prostate marked by activated Akt. To address whether KO mice exhibit increased skin carcinogenesis, WT and KO C57BL/6 mice were treated topically with 12‐<jats:italic>O</jats:italic>‐tetradecanoylphorbol‐13‐acetate and 7,12‐dimethylbenzanthracene. Compared to WT mice, KO mice developed squamous papillomas more rapidly and in greater numbers and also exhibited significantly increased progression to squamous cell carcinoma. Untreated KO epidermal layers were thicker than those in age‐matched WT mice and exhibited significantly increased levels of FAK and phospho‐ERK1/2, known mediators of carcinogen‐induced squamous papilloma progression to carcinoma. Compared to protein levels in WT mouse embryo fibroblasts (MEF), SSeCKS levels were increased in FAK‐null cells, whereas FAK levels were increased in SSeCKS‐null cells. RNAi studies in WT MEF cells suggest that SSeCKS and FAK attenuate each other's expression. Our study implicates a role for SSeCKS in preventing of skin cancer progression possibly through negatively regulating FAK expression.</jats:p> Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation International Journal of Cancer |
| spellingShingle | Akakura, Shin, Bouchard, Rene, Bshara, Wiam, Morrison, Carl, Gelman, Irwin H., International Journal of Cancer, Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation, Cancer Research, Oncology |
| title | Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_full | Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_fullStr | Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_full_unstemmed | Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_short | Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| title_sort | carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the ssecks/akap12 metastasis suppressor correlate with fak upregulation |
| title_unstemmed | Carcinogen‐induced squamous papillomas and oncogenic progression in the absence of the SSeCKS/AKAP12 metastasis suppressor correlate with FAK upregulation |
| topic | Cancer Research, Oncology |
| url | http://dx.doi.org/10.1002/ijc.25828 |