Publication: Anticancer effect of benzyl isothiocyanate on the apoptosis of human gemcitabine-resistant pancreatic cancer MIA PaCa-2/GemR cells (MIA RG100)
| cris.lastimport.scopus | 2026-02-28T16:01:40Z | |
| dc.creator | Hsueh, Chao-Wen | |
| dc.creator | Chen, Chun | |
| dc.creator | Chiu, Po-Yen | |
| dc.creator | Chiang, Ni-Na | |
| dc.creator | Lu, Chi-Cheng | |
| dc.creator | Yang, Jai-Sing | |
| dc.creator | Chen, Fu-An | |
| dc.date | 2022-07 | |
| dc.date.accessioned | 2023-05-02T08:59:40Z | |
| dc.date.accessioned | 2025-07-27T15:07:44Z | |
| dc.date.available | 2023-05-02T08:59:40Z | |
| dc.date.issued | 2023-05-02T08:59:40Z | |
| dc.description.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. | |
| dc.format.extent | 102 bytes | |
| dc.format.mimetype | text/html | |
| dc.identifier.doi | 10.4103/pm.pm_101_22 | |
| dc.identifier.issn | 0976-4062 | |
| dc.identifier.uri | https://ir.ntus.edu.tw/handle/987654321/64902 | |
| dc.language | en_US | |
| dc.publisher | Maharashtra, INDIA: WOLTERS KLUWER MEDKNOW PUBLICATIONS | |
| dc.relation | PHARMACOGNOSY MAGAZINE, 18(79), p.675-678 | |
| dc.subject | Apoptosis; | |
| dc.subject | benzyl isothiocyanate (BITC) | |
| dc.subject | gemcitabine-resistant pancreatic cancer cells (PaCa-2; GemR) | |
| dc.title | Anticancer effect of benzyl isothiocyanate on the apoptosis of human gemcitabine-resistant pancreatic cancer MIA PaCa-2/GemR cells (MIA RG100) | |
| dc.type | article | |
| dspace.entity.type | Publication |