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作者 Johnson, Tara Bardsley
書名 Effects of isoflavones and glycolytic enzyme inhibitors on regulation of proliferation and signaling pathways in oral squamous cell carcinoma cells (SCC15, SCC25): A mechanistic study
國際標準書號 9780549123262
book jacket
說明 94 p
附註 Source: Dissertation Abstracts International, Volume: 68-07, Section: B, page: 4413
Adviser: Alok Bhushan
Thesis (Ph.D.)--Idaho State University, 2007
Oral squamous cell carcinoma (OSCC) is the most common neoplasm of the head and neck. Worldwide, the annual incidence of new cases exceeds 350,000. The disease causes great morbidity, and the five-year survival rate of less than 50 percent has not improved in more than two decades. Chemoprevention of OSCC is based on two conditions---prevention of malignant conversion of premalignant lesions and prevention or reduction of local recurrences and in the rate of second primary lesions. Oral squamous carcinogenesis is a multistep process in which multiple genetic events occur that by which normal functions of oncogenes and tumor suppressor genes are altered resulting in increased production of growth factors or numbers of cell surface receptors, enhanced intracellular messenger signaling, and/or increased production of transcription factors. Advances in the molecular control of these various pathways may lead the way for novel approaches to treatment and prevention. The aims of these studies were to examine the molecular mechanisms mediating oral cancer progression and the effects of isoflavones and glycolytic enzyme inhibitors on OSCC
We investigated the effect of genistein and biochanin A on two oral cancer cell lines, SCC15 and SCC25. We examined the effect of these isoflavones on molecular mechanisms driving cell survival and proliferation in OSCC (e.g., mitogen-activated protein kinases (MAPK) and PI3K/Akt pathways, both known to be upregulated). Additionally, we investigated the effects of glycolytic enzyme inhibitors, 3-bromopyruvate and iodoactate, alone, and in combination with biochanin A, on proliferation, cell survival and cell death, and the PI3K/Akt pathway
Our results show that both genistein and biochanin A inhibited SCC15 and SCC25 cell growth. They also indicate that isoflavones inhibit the protein expression of phosphorylated ERK/MAPK and Akt. Moreover, our studies demonstrate that treatment with selective inhibitors of glycolytic enzymes, alone or in combination with biochanin A, induced death in OSCC cells and an inhibition of the Akt signaling pathway as one underlying cell signaling mechanism. Thus, our results may have pathophysiologic and pathogenetic implications in tumorogenesis of OSCC
School code: 0320
DDC
Host Item Dissertation Abstracts International 68-07B
主題 Health Sciences, Pharmacology
0419
Alt Author Idaho State University
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