Dehydroepiandrosterone induces growth arrest of hepatoma cells via alteration of mitochondrial gene expression and function

  • Authors:
    • Hung-Yao Ho
    • Mei-Ling Cheng
    • Hsin-Yu Chiu
    • Shiue-Fen Weng
    • Daniel Tsun-Yee Chiu
  • View Affiliations

  • Published online on: November 1, 2008     https://doi.org/10.3892/ijo_00000084
  • Pages: 969-977
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Abstract

DHEA is known to have anti-proliferative effect. The mechanism is not completely understood. We investigated the mechanism underlying DHEA-induced growth arrest of hepatoma cells. Growth inhibition was associated with increased G6PD activity, and insensitive to reversal by mevalonate. Thus, DHEA does not act via inhibition of G6PD and HMGR. Instead, growth stagnation was accompanied by reduced expression of nucleus-encoded mitochondrial genes; morphological and functional alterations of mitochondria; and depletion of intracellular ATP. Conversely, pyruvate supplementation alleviated DHEA-induced growth inhibition. It is likely that DHEA suppresses cell growth by altering mitochondrial gene expression, morphology and functions.

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November 2008
Volume 33 Issue 5

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Ho H, Cheng M, Chiu H, Weng S and Chiu DT: Dehydroepiandrosterone induces growth arrest of hepatoma cells via alteration of mitochondrial gene expression and function. Int J Oncol 33: 969-977, 2008
APA
Ho, H., Cheng, M., Chiu, H., Weng, S., & Chiu, D.T. (2008). Dehydroepiandrosterone induces growth arrest of hepatoma cells via alteration of mitochondrial gene expression and function. International Journal of Oncology, 33, 969-977. https://doi.org/10.3892/ijo_00000084
MLA
Ho, H., Cheng, M., Chiu, H., Weng, S., Chiu, D. T."Dehydroepiandrosterone induces growth arrest of hepatoma cells via alteration of mitochondrial gene expression and function". International Journal of Oncology 33.5 (2008): 969-977.
Chicago
Ho, H., Cheng, M., Chiu, H., Weng, S., Chiu, D. T."Dehydroepiandrosterone induces growth arrest of hepatoma cells via alteration of mitochondrial gene expression and function". International Journal of Oncology 33, no. 5 (2008): 969-977. https://doi.org/10.3892/ijo_00000084