ArticleJournal of cancer research and clinical oncology2008
SCC-112 gene is involved in tumor progression and promotes the cell proliferation in G2/M phase.
Article in Journal of cancer research and clinical oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
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- The proteomic investigation of chromatin functional domains reveals novel synergisms among distinct heterochromatin components.Molecular & cellular proteomics : MCP · 2013Article
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- Generation of expression vectors for high-throughput functional analysis of target genes in Schizosaccharomyces pombe.Journal of microbiology (Seoul, Korea) · 2009Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSCC-112 is a novel cell cycle-related gene and differentially expressed in cancers. Suggesting the complex role of SCC-112 might be existent in cell proliferation and tumor development. The relative research on SCC-112 has been few so far. This study is attempted to explore the role of SCC-112 in tumorigenesis. EXPERIMENTAL
designRT-PCR and western blot were performed on seven tumor-normal paired tissues and nine cell lines. Immunohistochemistry was carried out for analyzing the expression of SCC-112 in nasopharyngeal tissues. 293T and three nasopharyngeal cell lines were transfected with expression vector (pCMV-SPORT6-SCC-112) or its siRNA. Cell proliferation was examined by MTT and clone formation experiments. Immunoprecipitation determined the interacted protein of SCC-112, and FACS detected cell cycle parameter on cells treated with synchronized reagent.
resultsSCC-112 ( approximately 150 kDa) is up-regulated in tumor tissue as compared to the corresponding normal tissue and was detected in the tested cell lines. Overexpression of SCC-112 ( approximately 150 kDa) in 293T and three nasopharyngeal cell lines promoted cell proliferation and clone formation while downregulation of SCC-112 ( approximately 150 kDa) in these cells resulted in the opposite. Moreover, SCC-112 was found to interact with p63 and overexpression of SCC-112 up-regulated p63 expression. SCC-112 expression level positively correlated with cells in G2/M phase.
conclusionsThese findings suggest that SCC-112 improve cell proliferation and contributes to tumorigenesis by interacting with p63 and promoting cell cycling. SCC-112 might be an alternative target in tumor biomarking and mechanistic investigation.
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