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Int J Oncol. 2015;46(6):2606-12. doi: 10.3892/ijo.2015.2972. Epub 2015 Apr 20.

Downregulation of Sp1 is involved in β-lapachone-induced cell cycle arrest and apoptosis in oral squamous cell carcinoma.

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Department of Oral Pharmacology, School of Dentistry and Institute of Oral Bioscience, BK21 plus, Chonbuk National University, Jeonju 561-756, Republic of Korea.
Pohang Center for Evaluation of Biomaterials, Pohang, Gyeongbuk 790‑834, Republic of Korea.
Department of Pharmacy, College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Jeonnam 534-729, Republic of Korea.
Department of Biochemistry, Dongeui University College of Oriental Medicine, Busan 614-052, Republic of Korea.
Department of Animal Science and Technology, Sunchon National University, Suncheon, Republic of Korea.
Department of Animal Science, College of Agricultural and Life Science, Chonbuk National University, Jeonju 651-756, Republic of Korea.


β-lapachone (β-lap) is a naturally occurring quinone obtained from the bark of lapacho tree (Tabebuia avellanedae) with anti-proliferative properties against various cancers. The present study investigated the cell proliferation and apoptosis effect of β-lap on two oral squamous cell carcinoma lines (OSCCs). We carried out a series of 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl-2H-tetrazolium (MTS) assays, 4',6-diamidino-2-phenylindole (DAPI) staining, cell cycle analysis, and western blot analysis to characterize β-lap and its underlying signaling pathway. We demonstrated that β-lap-treated cells significantly reduced cell proliferation but increased DNA condensation and increased sub-G1 population in OSCCs. Particularly, β-lap suppresses activation of transcription factor specificity protein 1 (Sp1) followed by apoptosis in a concentration-dependent manner in OSCCs. Furthermore, β-lap modulated protein expression levels of cell cycle regulatory proteins and apoptosis-related proteins that are known as Sp1 target genes, resulting in apoptosis. Our results collectively indicated that β-lap was able to modulate Sp1 transactivation and induce apoptosis through the regulation of cell cycle and apoptosis-related proteins. Therefore, β-lap may be used in cancer prevention and therapies to improve clinical outcome as an anticancer drug candidate.

[Indexed for MEDLINE]

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