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p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers
Background: Concerted alterations between stromal fibroblasts and neoplastic cells underline the carcinogenic process. Activation of alpha-smooth muscle actin (SMA) expression, a cytoskeleton protein normally expressed only in myoepithelial cells, is considered a landmark for the activation of strom...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
IOS Press
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4605708/ https://www.ncbi.nlm.nih.gov/pubmed/20966541 http://dx.doi.org/10.3233/ACP-CLO-2010-0528 |
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author | Chatzistamou, Ioulia Dioufa, Nikolina Trimis, George Sklavounou, Alexandra Kittas, Christos Kiaris, Hippokratis Papavassiliou, Athanasios G. |
author_facet | Chatzistamou, Ioulia Dioufa, Nikolina Trimis, George Sklavounou, Alexandra Kittas, Christos Kiaris, Hippokratis Papavassiliou, Athanasios G. |
author_sort | Chatzistamou, Ioulia |
collection | PubMed |
description | Background: Concerted alterations between stromal fibroblasts and neoplastic cells underline the carcinogenic process. Activation of alpha-smooth muscle actin (SMA) expression, a cytoskeleton protein normally expressed only in myoepithelial cells, is considered a landmark for the activation of stromal fibroblasts with little however being known regarding the mechanism governing the expression of SMA in the stroma. Methods: We have evaluated by immunohistochemistry the expression of SMA in the stroma of oral malignant and pre-malignant lesions, in association with the expression of p53 and p21 tumor suppressors that were shown previously to be deregulated and/or mutated in stromal fibroblasts of various cancers. The effects of p21 knockdown in SMA expression and cell migration and the mRNA levels of endogenous p21 in fibroblasts co-cultured with cancer cells were also assessed. Results: We found that both p21 and SMA expression was elevated in the stroma, but not the epithelium, of malignant as compared to pre-malignant lesions. We also noted that the expression of both was positively correlated, implying that SMA expression may be regulated by p21. Consistently with this notion we found that siRNA-mediated p21 suppression resulted in the reduction of SMA levels and also inhibited cell migration. Conclusion: Our results show that p21 deregulation is associated with the activation of stromal fibroblasts of oral cancers by a mechanism that involves the stimulation of SMA expression. |
format | Online Article Text |
id | pubmed-4605708 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | IOS Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-46057082015-12-13 p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers Chatzistamou, Ioulia Dioufa, Nikolina Trimis, George Sklavounou, Alexandra Kittas, Christos Kiaris, Hippokratis Papavassiliou, Athanasios G. Anal Cell Pathol (Amst) Other Background: Concerted alterations between stromal fibroblasts and neoplastic cells underline the carcinogenic process. Activation of alpha-smooth muscle actin (SMA) expression, a cytoskeleton protein normally expressed only in myoepithelial cells, is considered a landmark for the activation of stromal fibroblasts with little however being known regarding the mechanism governing the expression of SMA in the stroma. Methods: We have evaluated by immunohistochemistry the expression of SMA in the stroma of oral malignant and pre-malignant lesions, in association with the expression of p53 and p21 tumor suppressors that were shown previously to be deregulated and/or mutated in stromal fibroblasts of various cancers. The effects of p21 knockdown in SMA expression and cell migration and the mRNA levels of endogenous p21 in fibroblasts co-cultured with cancer cells were also assessed. Results: We found that both p21 and SMA expression was elevated in the stroma, but not the epithelium, of malignant as compared to pre-malignant lesions. We also noted that the expression of both was positively correlated, implying that SMA expression may be regulated by p21. Consistently with this notion we found that siRNA-mediated p21 suppression resulted in the reduction of SMA levels and also inhibited cell migration. Conclusion: Our results show that p21 deregulation is associated with the activation of stromal fibroblasts of oral cancers by a mechanism that involves the stimulation of SMA expression. IOS Press 2010 2010-05-10 /pmc/articles/PMC4605708/ /pubmed/20966541 http://dx.doi.org/10.3233/ACP-CLO-2010-0528 Text en Copyright © 2010 Hindawi Publishing Corporation and the authors. |
spellingShingle | Other Chatzistamou, Ioulia Dioufa, Nikolina Trimis, George Sklavounou, Alexandra Kittas, Christos Kiaris, Hippokratis Papavassiliou, Athanasios G. p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers |
title | p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers |
title_full | p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers |
title_fullStr | p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers |
title_full_unstemmed | p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers |
title_short | p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers |
title_sort | p21/waf1 and smooth-muscle actin α expression in stromal fibroblasts of oral cancers |
topic | Other |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4605708/ https://www.ncbi.nlm.nih.gov/pubmed/20966541 http://dx.doi.org/10.3233/ACP-CLO-2010-0528 |
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