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Increased chemoresistance by butyrate in human colon cancer cells
- Author(s)
- 강향리
- Advisor
- 김소희
- Department
- 일반대학원 약학
- Publisher
- The Graduate School, Ajou University
- Publication Year
- 2016-02
- Language
- eng
- Keyword
- Colon cancer; Butyrate; Chemoresistance; Apoptosis; HCT116 cells
- Alternative Abstract
- Butyrate is a short-chain fatty acid produced by intestinal microflora and it not only induces apoptosis, but also inhibits cell proliferation in cancer. Recently, it has been reported butyrate may cause resistance in colon cancer. So we investigated the effects of increased resistance to butyrate in HCT116 colon cancer cells. We established HCT116 cells resistant to butyrate (HCT116/BR) by treating HCT116 parental cells (HCT116/PT) with increasing the concentration of butyrate gradually up to 1.6 mM for three months. The concentrations inhibiting the cell growth by 50% (IC50) of butyrate were 0.508 and 5.50 mM in HCT116/PT and HCT116/BR. The values of IC50 after the treatment with paclitaxel, 5-fluorouracil (5-FU), doxorubicin or trichostatin A (TSA) were 2.42, 2.36, 4.31 and 11.3 fold higher, respectively, in HCT116/BR cells compared with HCT116/PT cells. The protein expression of drug efflux pumps such as P-glycoprotein (P-gp), breast cancer resistant protein (BCRP) and the multidrug resistance associated protein 1 (MRP1) were not changed between HCT116/PT and HCT116/BR cells. The expressions of anti-apoptotic Bcl-xL protein were increased while those of pro-apoptotic Bax and Bim proteins were reduced in HCT116/BR cells. There were no significant differences in cell motility and invasion. Our study suggests that when colon cancer cells are exposed to butyrate consistently, cancer cells can have resistance to butyrate which may play a role in acquisition of chemoresistance in colon cancer.
- Fulltext
- Appears in Collections:
- Graduate School of Ajou University > Department of Pharmacy > 3. Theses(Master)
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