Project description:Previous studies indicated TCAB1, also known as WRAP53, had oncogenic feature in a certain extend. However, there is none direct study on the function of TCAB1 in tumorigenesis and development of head and neck cancers. First of all, we verified the function of TCAB1 in head and neck cancers. Knockdown TCAB1 would inhibit cell proliferation in Vitro as well as in Vivo, meanwhile, depletion TCAB1 would decrease the invasion potential of OSCC Cal-27 cells. cDNA microarray analysis showed many pathways and factors associated with occurrence and development of carcinomas were implicated in this process. Our study indicated TCAB1 might be a potential target for prognosis and therapy in head and neck cancers.
Project description:This SuperSeries is composed of the following subset Series: GSE11929: Identification of a subgroup of head and neck cancers lacking numerical chromosomal aberrations GSE11931: Copy Number Alterations in HNSCC with or without Oncogene Expressing Human Papillomavirus Refer to individual Series
Project description:Previous studies indicated TCAB1, also known as WRAP53, had oncogenic feature in a certain extend. However, there is none direct study on the function of TCAB1 in tumorigenesis and development of head and neck cancers. First of all, we verified the function of TCAB1 in head and neck cancers. Knockdown TCAB1 would inhibit cell proliferation in Vitro as well as in Vivo, meanwhile, depletion TCAB1 would decrease the invasion potential of OSCC Cal-27 cells. cDNA microarray analysis showed many pathways and factors associated with occurrence and development of carcinomas were implicated in this process. Our study indicated TCAB1 might be a potential target for prognosis and therapy in head and neck cancers. Immunohistochemistry assay and western blot showed TCAB1 was overexpressed in clinical nasopharyngeal carcinoma and head and neck cell lines. Depletion endogenous TCAB1 by shRNA lentivirus in Cal-27 would verify the function of TCAB1 in cells proliferation and invasion. Furthermore, cDNA microarray was performed to detect some pathways or factors involved in the process.
Project description:The critical role of Bmi1 in promoting stem cell properties has been shown in different type of human cancers. Here, we established four stable clones to study Bmi-regulated miRNA expression patterns in head and neck caners.
Project description:Solid tumors, including head and neck squamous cell carcinomas (HNSCC), arise as a result of genetic and epigenetic alterations in a sustained stress environment. Since it has been hypothesized that epigenetic alterations may act by providing the second carcinogenic hit in gene silencing, we sought to identify genome-wide DNA copy number alterations and CpG dinucleotide methylation events and examine the global/local relationships between these types of alterations in HNSCC. Importantly, we found that the global pattern of copy number alterations in these tumors was significantly associated with tumor methylation profiles. However at the local level, gene promoter regions did not exhibit a correlation between copy number and methylation , and the spectrum of genes affected by each type of alteration was unique. A case-series of 19 tumors and matched blood referents were hybrizided to Affymetrix Human Mapping 500k arrays and copy number was determined via HMM with Copy Number Analysis Tool v4.0.1. This study was designed to investigate the relationship between copy number and DNA methylation alterations in head and neck squamous cell carcinoma. Data in this submission relates to the methylation portion only. Each patient tumor has been de-identified and assigned a number (1-19). We included 11 normal head and neck samples, procured through the National Research Disease Interchange, that were used for reference when comparing tumor to normal. One ug of tissue DNA extracted using the Qiagen Blood and Tissue Kit was bisulfite-modified using a Zymo Research EZ DNA Methylation Kit. Samples were processed and arrayed on the Illumina GoldenGate Methylation Cancer Panel 1 at the University of California-San Francisco Institute for Genetics, Genomic Core Facility.