| Regulation of motility, invasion, and metastatic potential of squamous cell carcinoma by 1α,25-dihydroxycholecalciferol. | |
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MedLine Citation:
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PMID: 22833444 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The active metabolite of vitamin D 1α,25-dihydroxycholecalciferol (1,25D(3) ) has exhibited broad-spectrum antitumor activity in xenograft animal models. However, its activity against metastatic disease has not been extensively investigated. METHODS: Squamous cell carcinoma (SCC) or 1,25D(3) -resistant variant SCC-DR cells were treated with 1,25D(3) . Actin organization was examined by immunofluorescence assay. Cell migration was assessed by "wound" healing and chemotactic migration assays. Cell invasion was assessed by a Matrigel-based invasion assay and in situ zymography. Matrix metalloproteinase 2 (MMP-2) and MMP-9 expression and secretion were examined by immunoblot analysis and an enzyme-linked immunosorbent assay, respectively. E-cadherin expression was assessed by flow cytometry, immunoblot analysis, and immunohistochemistry. Knockdown of E-cadherin was achieved by small interfering RNA. An experimental metastasis mouse model was created by intravenous injection of tumor cells; and lung tumor development in the mice was assessed by magnetic resonance imaging, gross observation, and histology. RESULTS: SCC cellular morphology and actin organization were altered by 10 nM 1,25D(3) . 1,25D(3) inhibited SCC cell motility and invasion, which were associated with reduced expression and secretion of MMP-2 and MMP-9, and 1,25D(3) promoted the expression of E-cadherin. These findings were not observed in SCC-DR cells. Knock down of E-cadherin rescued 1,25D(3) -inhibited cell migration. Intravenous injection of SCC or SCC-DR cells resulted in the establishment of extensive pulmonary lesions in saline-treated C3H mice. Treatment with 1,25D(3) resulted in a marked reduction in the formation of lung tumor colonies in mice that were injected with SCC cells, but not in mice that were injected with SCC-DR cells. CONCLUSIONS: 1,25D(3) suppressed SCC cell motility, invasion, and metastasis, partially through the promotion of E-cadherin-mediated cell-cell adhesion. |
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Authors:
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Yingyu Ma; Wei-Dong Yu; Bing Su; Mukund Seshadri; Wei Luo; Donald L Trump; Candace S Johnson |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-07-25 |
Journal Detail:
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Title: Cancer Volume: 119 ISSN: 1097-0142 ISO Abbreviation: Cancer Publication Date: 2013 Feb |
Date Detail:
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Created Date: 2013-01-23 Completed Date: 2013-03-21 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0374236 Medline TA: Cancer Country: United States |
Other Details:
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Languages: eng Pagination: 563-74 Citation Subset: AIM; IM |
Copyright Information:
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Copyright © 2012 American Cancer Society. |
Affiliation:
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Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cadherins / genetics, metabolism Calcitriol / pharmacology* Carcinoma, Squamous Cell / drug therapy, pathology* Cell Adhesion / drug effects, genetics Cell Line, Tumor Cell Movement / drug effects* Cell Shape / drug effects Drug Evaluation, Preclinical Gene Expression Regulation, Neoplastic / drug effects Lung Neoplasms / drug therapy, pathology*, secondary Mice Mice, Inbred C3H Neoplasm Invasiveness Neoplasm Metastasis Neoplasm Transplantation |
| Grant Support | |
ID/Acronym/Agency:
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CA067267/CA/NCI NIH HHS; CA085142/CA/NCI NIH HHS; CA095045/CA/NCI NIH HHS; P30CA16056/CA/NCI NIH HHS; R01 CA067267/CA/NCI NIH HHS; R01 CA067267-18/CA/NCI NIH HHS; R01 CA085142-10/CA/NCI NIH HHS; R01 CA095045-09/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cadherins; 32222-06-3/Calcitriol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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