@Article{096504015X14424348426071,
AUTHOR = {Wunchana Seubwai, Kulthida Vaeteewoottacharn, Ratthaphol Kraiklang,
Kazuo Umezawa, Seiji Okada, Sopit Wongkham},
TITLE = {Inhibition of NF-kB Activity Enhances Sensitivity to Anticancer Drugs in Cholangiocarcinoma Cells},
JOURNAL = {Oncology Research},
VOLUME = {23},
YEAR = {2015},
NUMBER = {1-2},
PAGES = {21--28},
URL = {http://www.techscience.com/or/v23n1-2/57566},
ISSN = {1555-3906},
ABSTRACT = {Cholangiocarcinoma (CCA) is a dismal cancer. At present, there is no effective chemotherapeutic regimen 
for CCA. This may be due to the marked resistance of CCA to chemotherapy drugs, for which a mechanism 
remains unknown. Nuclear factor-kB (NF-kB) is constitutively activated in a variety of cancer cells, including 
CCA. It has been shown to play roles in growth, metastasis, and chemoresistance of cancer. In the present study, 
we examined whether NF-kB is involved in the chemoresistance of CCA and whether dehydroxymethylepoxyquinomicin (DHMEQ), an effective NF-kB inhibitor, can overcome the drug resistance of CCA. Two CCA cell 
lines, KKU-M213 and KKU-M214, were treated with DHMEQ and/or chemotherapeutic drugs. Cell viability, 
apoptosis, and the expressions of the ATP-binding cassette (ABC) transporters were compared. The combination of chemotherapy drugs, 5-fluorouracil, cisplatin, and doxorubicin, with DHMEQ significantly enhanced 
the cytotoxicity of all chemotherapeutic drugs compared to DHMEQ or drug alone. Furthermore, the mRNA 
level of ABCB1, a multidrug-resistant protein, was significantly decreased in the 5-fluorouracil combined with 
DHMEQ-treated cells. These findings suggest that the inhibition of NF-kB by DHMEQ enhanced the chemoresponsiveness of CCA cells, possibly by reducing the expression of ABC transporter. Inhibition of NF-kB may 
be a potential chemodrug-sensitizing strategy for chemoresistant cancer such as CCA.},
DOI = {10.3727/096504015X14424348426071}
}