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Cancer Chemoprevention Effects of Geldanamycin and 17-AAG in Human Oral Squamous Cell Carcinoma
Korean J Clin Lab Sci 2018;50:462-469  
Published on December 31, 2018
Copyright © 2018 Korean Society for Clinical Laboratory Science.

Eun Ju Lee

Department of Clinical Laboratory Science, Daejeon Health Science College, Daejeon, Korea
Correspondence to: Eun Ju Lee
Department of Clinical Laboratory Science, Daejeon Health Science College, 21 Chungjeong-ro, Dong-gu, Daejeon 34504, Korea
Tel: 82-42-670-9163 Fax: 82-42-670-9160 E-mail:
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
HSP90 regulates various proteins involved in differentiation and cell survival. Levels of HSP90 tend to increase during development of squamous cell carcinoma in the head and neck including the mouth. Thus, many studies have been conducted to treat these cancers through suppression of HSP90. This study investigated the effect of two HSP90 inhibitors, geldanamycin and 17-AAG, on the proliferation, apoptosis, and invasion of human oral squamous cell carcinoma cells. Cell survival and cell cycle analyses, as well as western blot analysis, were performed with oral cancer cell lines, YD-10B and YD-38. After treatment with HSP90 inhibitors, cell proliferation was significantly inhibited. When YD-10B and YD-38 cells were treated with various concentrations of geldanamycin and 17-AAG (0, 0.1, 0.3, 1 and 10 μM) for 24 hr, the growth of YD-10B cells was markedly reduced compared to that of YD-38 cells. Thereafter, the cells were subjected to flow cytometry, which revealed G2 arrest. These results demonstrated that geldanamycin induced G2 arrest and inhibited cell proliferation through the p-GSK-3β pathway in YD-10B and YD-38 cells, thus inhibiting cell survival. HSP90 inhibitors are therefore expected to have a therapeutic effect on various cancer cell lines.
Keywords : Cell proliferation, Geldanamycin, Glycogen synthase kinase 3-beta

December 2018, 50 (4)
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