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|Title: ||Nm23-H1 Regulates Mitochondrial Bioenergetic Function in Human Head and Neck Squamous Cell Carcinoma SAS Cells|
|Authors: ||Lin YK;Wang YF;Chen YJ;Chen CT;Wu SB;Wei YH;Chang CJ|
|Contributors: ||NTOU:Department of Food Science|
|Issue Date: ||2011-10-21T02:24:58Z
|Publisher: ||The 2010 Workshop on Recent Advances in Bioenergetics and Mitochondrial Medicine (Taipei, Taiwan. Sep. 10-12, 2010). Fourth Place Award|
|Abstract: ||Abstract:Background & Aim Nm23 (non-metastatic clone 23) is known to be a multifunctional protein, acting as a metastasis suppressor with transactivation activity on c-myc and regulating endocytosis in human cells. However, how Nm23 exerts the wide spectrum of cellular activities and how these activities are regulated are not well understood. Eight distinct isotypes of human Nm23 (Nm23-H1 to -H8) have been identified to date. This study was launched to investigate the role of mitochondria in the Nm23-H1-mediated malignancy of head and neck squamous cell carcinoma (HNSCC) cells. Methods & Results By the established in vitro models of HNSCC SAS cell lines with stable Nm23-H1 overexpression and knockdown, our recent studies revealed that knockdown of Nm23-H1 resulted in chemo-resistance and increased transwell invasion of HNSCC cells. Decrease in mitochondrial oxidative phosphorylation and availability of ATP associated with malignancies have been reported in various human cancer cells. We found that knockdown of Nm23-H1 resulted in a decrease of mitochondrial membrane potential, but has no significant effects on mitochondrial mass and production of H2O2 in HNSCC cells. Upon treatment with oligomycin (inhibitor of the ATP synthase), the oxygen consumption rate (OCR) was significantly declined in wild-type and Nm23-H1 knockdown cells, but not in cells with Nm23-H1 overexpression. These results indicate that Nm23-H1 is involved in the maintenance of aerobic metabolism when the availability of ATP is reduced in HNSCC cells. On the other hand, we found that cells with Nm23-H1 overexpression showed lower levels of extracellular acidification rate (ECAR) upon treatment with oligomycin. This suggests that the Nm23-H1 knockdown cells rely more on glycolysis for energy supply compared with cells overexpressing Nm23-H1. The mechanism of Nm23-H1-regulated mitochondrial bioenergetic function and attenuated dependence on glycolysis in relation to the malignancy of HNSCC cel|
|Relation: ||Poster no. C-03|
|Appears in Collections:||[食品科學系] 演講及研討會|
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