ArticleCellular oncology (Dordrecht, Netherlands)2011
p21/waf1 and smooth-muscle actin α expression in stromal fibroblasts of oral cancers.
Article in Cellular oncology (Dordrecht, Netherlands), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- A tumor microenvironment gene set-Based prognostic signature for non-small-cell lung cancer.Frontiers in molecular biosciences · 2022Article
- Quantitative proteomic profiling of primary cancer-associated fibroblasts in oesophageal adenocarcinoma.British journal of cancer · 2018Article
- A CCL8 gradient drives breast cancer cell dissemination.Oncogene · 2016Article
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- Overexpression p21WAF1/CIP1 in suppressing retinal pigment epithelial cells and progression of proliferative vitreoretinopathy via inhibition CDK2 and cyclin E.BMC ophthalmology · 2014Article
- Autophagy and senescence in cancer-associated fibroblasts metabolically supports tumor growth and metastasis via glycolysis and ketone production.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
- Erratum issued
- Reprint of
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundConcerted 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.
methodsWe 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.
resultsWe 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.
conclusionOur 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.
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