Article · Volume 18, Issue 79 · pp. 675–678
Anticancer Effect of Benzyl Isothiocyanate on the Apoptosis of Human Gemcitabine‑Resistant Pancreatic Cancer MIA PaCa‑2/ GemR Cells (MIA RG100)
Chao‑Wen Hsueh1, Chun Chen2, Po‑Yen Chiu3, Ni‑Na Chiang4, Chi‑Cheng Lu5, Jai‑Sing Yang6, Fu‑An Chen3
- 1Department of Internal Medicine, Division of Gastroenterology, Kaohsiung Armed Forces General Hospital, Kaohsiung 802, Taiwan.
- 2School of Pharmacy, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
- 3Department of Pharmacy and Master Program, Tajen University, Pingtung 907, Taiwan.
- 4Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.
- 5Department of Sport Performance, National Taiwan University of Sport, Taichung 404, Taiwan.
- 6Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan.
Abstract
Background: Benzyl isothiocyanate (BITC) is a natural compound found in numerous cruciferous vegetables, and research has indicated that it has diverse biological activities. Isothiocyanate and its derivatives are the major anticancer natural compounds in cruciferous vegetables; these compounds help inhibit tumor cell proliferation through various mechanisms such as promoting tumor cell apoptosis, prompting cycle arrest, and increasing the generation of reactive oxygen species (ROS).Objectives: In human pancreatic cancer, gemcitabine is the first‑line treatment; however, pancreatic cancer cells readily develop resistance to gemcitabine. Studies have demonstrated that natural products can promote the effect of gemcitabine and enhance the apoptosis process; however, the relevant mechanism and potential of BITC in human pancreatic cancer cells with gemcitabine resistance, namely, MIA PaCa‑2/GemR cells (MIA RG100), are unclear.Materials and Methods: To elucidate the extent to which BITC induces apoptosis, we investigated the time and dose‑dependent cell viability of PaCa‑2/GemR cells under treatment with BITC.Results: Following BITC treatment, the PaCa‑2/GemR cells exhibited DNA condensation, as indicated by transferase‑mediated d‑UTP nick end labeling (TUNEL) stain, with a corresponding increase in ROS production in mitochondria. Moreover, colorimetric assay analyses revealed that BITC increased caspase‑9 and caspase‑3 activities in PaCa‑2/GemR cells. Our results indicate that BITC induces apoptotic cell death in PaCa‑2/GemR cells through a mitochondrial‑dependent signaling pathway.
Keywords: Apoptosis; benzyl isothiocyanate (BITC); gemcitabine‑resistant pancreatic cancer cells (PaCa‑2/GemR)
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