Coptidis Rhizoma Extract Reverses 5-Fluorouracil Resistance in HCT116 Human Colorectal Cancer Cells via Modulation of Thymidylate Synthase

被引:17
作者
Kang, Yong-Hwi [1 ]
Lee, Jin-Seok [1 ]
Lee, Nam-Hun [2 ]
Kim, Seung-Hyung [3 ]
Seo, Chang-Seob [4 ]
Son, Chang-Gue [1 ]
机构
[1] Daejeon Univ, Daejeon Oriental Hosp, Inst Biosci & Integrat Med, Daejeon 35353, South Korea
[2] Daejeon Univ, Cheonan Oriental Hosp, Dept Clin Oncol, 4 Notaesan Ro, Cheonan Si 31099, South Korea
[3] Daejeon Univ, Inst Tradit Med & Biosci, Daehak Ro 62, Daejeon 34520, South Korea
[4] Korea Inst Oriental Med, Herbal Med Res Div, Res Infrastruct Team, 1672 Yuseong Daero, Daejeon 34054, South Korea
基金
新加坡国家研究基金会;
关键词
colorectal cancer; chemoresistance; 5-fluorouracil; thymidylate synthase; Coptidis rhizoma; DRUG-RESISTANCE; OXALIPLATIN; FLUOROURACIL; RESVERATROL; MECHANISMS; EXPRESSION; IRINOTECAN; SURVIVAL;
D O I
10.3390/molecules26071856
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Colorectal cancer (CRC) is a malignancy of the colon or rectum. It is ranked as the third most common cancer in both men and women worldwide. Early resection permitted by early detection is the best treatment, and chemotherapy is another main treatment, particularly for patients with advanced CRC. A well-known thymidylate synthase (TS) inhibitor, 5-fluorouracil (5-FU), is frequently prescribed to CRC patients; however, drug resistance is a critical limitation of its clinical application. Based on the hypothesis that Coptidis Rhizoma extract (CRE) can abolish this 5-FU resistance, we explored the efficacy and underlying mechanisms of CRE in 5-FU-resistant (HCT116/R) and parental HCT116 (HCT116/WT) cells. Compared to treatment with 5-FU alone, combination treatment with CRE and 5-FU drastically reduced the viability of HCT116/R cells. The cell cycle distribution assay showed significant induction of the G0/G1 phase arrest by co-treatment with CRE and 5-FU. In addition, the combination of CRE and 5-FU notably suppressed the activity of TS, which was overexpressed in HCT116/R cells, as compared to HCT116/WT cells. Our findings support the potential of CRE as an adjuvant agent against 5-FU-resistant colorectal cancers and indicate that the underlying mechanisms might involve inhibition of TS expression.
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页数:12
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