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Transcription profiling of human head and neck squamous cell carcinoma samples reveals a feed-forward loop involving protein kinase Calpha and microRNAs regulates tumor cell cycle

ABSTRACT: Patient selection and specimen collection. Thirty-six freshly frozen tumor samples were prospectively collected from patients undergoing surgery or biopsy for HNSCC at the University of North Carolina (UNC) at Chapel Hill (21 patients) and Vanderbilt University (15 patients). All tissues were snap-frozen in liquid nitrogen within 30 minutes of surgical resection or biopsy, and kept at -80oC until further processing. All patients consented to participation in this study under protocols approved by IRB at the two institutions. This set includes the samples previously deposited into GEO including 8 additional samples and adjustment for protocol changes. The original 36 before protocol changes (and thus unadjusted) are here: Slebos RJ, Yi Y, Ely K, et al. Gene expression differences associated with human papillomavirus status in head and neck squamous cell carcinoma. Clin Cancer Res 2006;12(3 Pt 1):701-9. Experiment Overall Design: 44 primary head and neck tumor samples

ORGANISM(S): Homo sapiens

SUBMITTER: Christine Chung 

PROVIDER: E-GEOD-10300 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A feed-forward loop involving protein kinase Calpha and microRNAs regulates tumor cell cycle.

Cohen Ezra E W EE   Zhu Hongyan H   Lingen Mark W MW   Martin Leslie E LE   Kuo Wen-Liang WL   Choi Eugene A EA   Kocherginsky Masha M   Parker Joel S JS   Chung Christine H CH   Rosner Marsha Rich MR  

Cancer research 20090101 1

Protein kinase Calpha (PKCalpha) has been implicated in cancer, but the mechanism is largely unknown. Here, we show that PKCalpha promotes head and neck squamous cell carcinoma (SCCHN) by a feed-forward network leading to cell cycle deregulation. PKCalpha inhibitors decrease proliferation in SCCHN cell lines and xenografted tumors. PKCalpha inhibition or depletion in tumor cells decreases DNA synthesis by suppressing extracellular signal-regulated kinase phosphorylation and cyclin E synthesis. A  ...[more]

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