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ORIGINAL ARTICLE
Year : 2022  |  Volume : 18  |  Issue : 79  |  Page : 675-678

Anticancer effect of benzyl isothiocyanate on the apoptosis of human gemcitabine-resistant pancreatic cancer MIA PaCa-2/GemR cells (MIA RG100)


1 Department of Internal Medicine, Division of Gastroenterology, Kaohsiung Armed Forces General Hospital, Kaohsiung 802, Taiwan
2 School of Pharmacy, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan
3 Department of Pharmacy and Master Program, Tajen University, Pingtung 907, Taiwan
4 Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan
5 Department of Sport Performance, National Taiwan University of Sport, Taichung 404, Taiwan
6 Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan

Correspondence Address:
Fu-An Chen
Department of Pharmacy and Master Program, Tajen University, 20 Weixin Road, Yanpu, Pingtung 907
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_101_22

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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.


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