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Article

Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells

  • Authors:
    • Mee-Young Ahn
    • Ji-Wee Ahn
    • Hyung-Sik Kim
    • Jun Lee
    • Jung-Hoon Yoon
  • View Affiliations / Copyright

    Affiliations: Department of Oral and Maxillofacial Pathology, College of Dentistry, Wonkwang Bone Regeneration Research Institute, Daejeon Dental Hospital, Wonkwang University, Daejeon 302-120, Republic of Korea, Division of Toxicology, School of Pharmacy, Sungkyunkwan University, Suwon 440-746, Republic of Korea, Department of Oral and Maxillofacial Surgery, College of Dentistry, Wonkwang Bone Regeneration Research Institute, Daejeon Dental Hospital, Wonkwang University, Daejeon 302-120, Republic of Korea
  • Pages: 1899-1907
    |
    Published online on: February 2, 2015
       https://doi.org/10.3892/or.2015.3776
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Abstract

Inhibition of histone deacetylases (HDACs) has emerged as a new target for cancer therapies. The present study examined the antitumor effect and molecular mechanism of the HDAC inhibitor apicidin in YD-15 human salivary mucoepidermoid carcinoma (MEC) cells. The cells were treated with apicidin and cell death was quantified using an MTT assay. Apoptosis and autophagy were measured using flow cytometry, immunoblot analysis and cell staining. Regulation of the signaling pathways was monitored using immunoblot analysis and co-treatment with specific inhibitors. Insulin-like growth factor 1 receptor (IGF-1R) was knocked down using specific siRNA. Apicidin significantly inhibited the proliferation of MEC cells. Apicidin also induced apoptosis through the inactivation of extracellular signal-regulated kinase (ERK) and AKT/mTOR signaling and activation of c-Jun NH2-terminal kinase (JNK), whereas apicidin promoted autophagy through inactivation of the AKT/mTOR signaling. These effects may be mediated by the inhibition of IGF-1R, an upstream regulator of MAPK and AKT/mTOR pathways. These results suggested that apicidin is an attractive chemotherapeutic agent against salivary MEC and may be a good candidate for targeting IGF-1R for cancer therapies.
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Copy and paste a formatted citation
Spandidos Publications style
Ahn M, Ahn J, Kim H, Lee J and Yoon J: Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells. Oncol Rep 33: 1899-1907, 2015.
APA
Ahn, M., Ahn, J., Kim, H., Lee, J., & Yoon, J. (2015). Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells. Oncology Reports, 33, 1899-1907. https://doi.org/10.3892/or.2015.3776
MLA
Ahn, M., Ahn, J., Kim, H., Lee, J., Yoon, J."Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells". Oncology Reports 33.4 (2015): 1899-1907.
Chicago
Ahn, M., Ahn, J., Kim, H., Lee, J., Yoon, J."Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells". Oncology Reports 33, no. 4 (2015): 1899-1907. https://doi.org/10.3892/or.2015.3776
Copy and paste a formatted citation
x
Spandidos Publications style
Ahn M, Ahn J, Kim H, Lee J and Yoon J: Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells. Oncol Rep 33: 1899-1907, 2015.
APA
Ahn, M., Ahn, J., Kim, H., Lee, J., & Yoon, J. (2015). Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells. Oncology Reports, 33, 1899-1907. https://doi.org/10.3892/or.2015.3776
MLA
Ahn, M., Ahn, J., Kim, H., Lee, J., Yoon, J."Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells". Oncology Reports 33.4 (2015): 1899-1907.
Chicago
Ahn, M., Ahn, J., Kim, H., Lee, J., Yoon, J."Apicidin inhibits cell growth by downregulating IGF-1R in salivary mucoepidermoid carcinoma cells". Oncology Reports 33, no. 4 (2015): 1899-1907. https://doi.org/10.3892/or.2015.3776
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