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Article

Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1

  • Authors:
    • Ra Ham Lee
    • Jae-Cheon Shin
    • Ka-Hwi Kim
    • Yung Hyun Choi
    • Jung-Il Chae
    • Jung-Hyun Shim
  • View Affiliations / Copyright

    Affiliations: Department of Oral Pharmacology, School of Dentistry and Institute of Oral Bioscience, BK21 plus, Chonbuk National University, Jeonju 651-756, Republic of Korea, Pohang Center for Evaluation of Biomaterials, Pohang Technopark, Jigok-dong, Pohang, Gyeongbuk 790-834, Republic of Korea, Natural Medicine Research Institute, Department of Pharmacy, College of Pharmacy, Mokpo National University, Muan-gun, Jeonnam 534-729, Republic of Korea, Department of Biochemistry, Dongeui University College of Oriental Medicine, Busan 614-052, Republic of Korea
  • Pages: 631-638
    |
    Published online on: November 27, 2014
       https://doi.org/10.3892/or.2014.3632
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Abstract

7,8-Dihydroxyflavone (7,8-DHF) is a member of the flavonoid family and has recently been identified as a brain-derived neurotrophic factor mimetic that selectively activates tropomyosin-receptor kinase B with high affinity. The antioxidant and anticancer effects of 7,8-DHF have been reported. However, the pharmacological mechanisms of 7,8-DHF in oral cancer are unclear. Thus, we investigated the mechanisms of the antiproliferative action of 7,8-DHF on HN22 and HSC4 oral squamous cell carcinoma cell lines. We demonstrated that 7,8-DHF decreased cell growth and induced apoptosis in the HN22 and HSC4 cells through regulation of specificity protein 1 (Sp1) using the MTS assay, DAPI staining, Annexin V, propidium iodide staining, reverse transcription-polymerase chain reaction, immunocytochemistry, pull-down assay and western blot analysis. The results showed that the Sp1 protein bound with 7,8-DHF in the HN22 and HSC4 cells. Taken together, the results suggest that 7,8-DHF could modulate Sp1 transactivation and induce apoptotic cell death by regulating the cell cycle and suppressing antiapoptotic proteins. Furthermore, 7,8-DHF may be valuable for cancer prevention and better clinical outcomes.
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Copy and paste a formatted citation
Spandidos Publications style
Lee RH, Shin J, Kim K, Choi YH, Chae J and Shim J: Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1. Oncol Rep 33: 631-638, 2015.
APA
Lee, R.H., Shin, J., Kim, K., Choi, Y.H., Chae, J., & Shim, J. (2015). Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1. Oncology Reports, 33, 631-638. https://doi.org/10.3892/or.2014.3632
MLA
Lee, R. H., Shin, J., Kim, K., Choi, Y. H., Chae, J., Shim, J."Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1". Oncology Reports 33.2 (2015): 631-638.
Chicago
Lee, R. H., Shin, J., Kim, K., Choi, Y. H., Chae, J., Shim, J."Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1". Oncology Reports 33, no. 2 (2015): 631-638. https://doi.org/10.3892/or.2014.3632
Copy and paste a formatted citation
x
Spandidos Publications style
Lee RH, Shin J, Kim K, Choi YH, Chae J and Shim J: Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1. Oncol Rep 33: 631-638, 2015.
APA
Lee, R.H., Shin, J., Kim, K., Choi, Y.H., Chae, J., & Shim, J. (2015). Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1. Oncology Reports, 33, 631-638. https://doi.org/10.3892/or.2014.3632
MLA
Lee, R. H., Shin, J., Kim, K., Choi, Y. H., Chae, J., Shim, J."Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1". Oncology Reports 33.2 (2015): 631-638.
Chicago
Lee, R. H., Shin, J., Kim, K., Choi, Y. H., Chae, J., Shim, J."Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1". Oncology Reports 33, no. 2 (2015): 631-638. https://doi.org/10.3892/or.2014.3632
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