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RETRACTED

BioMed Research International has retracted this article. As noted by Amanda Capes-Davis on PubMed Commons, KB cells are cross-contaminated by HeLa and are not oral cancer cells [2]. Therefore, the conclusions cannot be supported. Tan IIA was already known to induce apoptosis in HeLa cells through a mitochondria-dependent pathway [3].

BioMed Research International
Volume 2014 (2014), Article ID 540516, 7 pages
http://dx.doi.org/10.1155/2014/540516
Research Article

Tanshinone IIA Induces Apoptosis in Human Oral Cancer KB Cells through a Mitochondria-Dependent Pathway

1Department of Otorhinolaryngology, Head and Neck Surgery, Changhua Christian Hospital, No. 135 Nanxiao Street, Changhua 500, Taiwan
2Cancer Research Center, Changhua Christian Hospital, Changhua 500, Taiwan
3Institute of Medicine, Chung Shan Medical University, Taichung 500, Taiwan
4School of Optometry, Chung Shan Medical University, Taichung 402, Taiwan
5Department of Pharmacy, Changhua Christian Hospital, No. 135 Nanxiao Street, Changhua 500, Taiwan
6School of Pharmacy, China Medical University, Taichung 404, Taiwan
7College of Health Sciences, Chang Jung Christian University, Tainan 711, Taiwan

Received 26 February 2014; Accepted 12 April 2014; Published 13 May 2014

Academic Editor: Tsung-Lin Yang

Copyright © 2014 Pao-Yu Tseng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Tanshinone IIA (Tan IIA), an active phytochemical in the dried root of Salvia miltiorrhiza Bunge, has shown an antiproliferative activity on various human cancer cell lines including nasopharyngeal carcinoma cells. However, the effects of Tan IIA on human oral cancer cells are still unknown. This study aimed to investigate the antiproliferative effects of Tan IIA on human oral cancer KB cells and explored the possible underlying mechanism. Treatment of KB cells with Tan IIA suppressed cell proliferation/viability and induced cell death in a dose-dependent manner through sulforhodamine B colorimetric assay. Observation of cell morphology revealed the involvement of apoptosis in the Tan IIA-induced growth inhibition on KB cells. Cell cycle analysis showed a cell cycle arrest in G2/M phase on Tan IIA-treated cells. The dissipation of mitochondrial membrane potential observed by flow cytometry and the expression of activated caspases with the cleaved poly (ADP-ribose) polymerase under immunoblotting analysis indicated that Tan IIA-induced apoptosis in KB cells was mediated through the mitochondria-dependent caspase pathway. These observations suggested that Tan IIA could be a potential anticancer agent for oral cancer.