지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.12
- 수록면
- 131 - 137 (7page)
이용수
초록· 키워드
오류제보하기
Purpose: A water-soluble variant of the artemisinin called artesunate, approved as an antimalarial agent, can induce cell death on various cancer cell types. We studied the mechanism of cell death of artesunate on HCT116 colorectal cancer cells.
Methods: We treated HCT116 colon cancer cells with artesunate, holo-transferrin, deferoxamine mesylate, ferrostatin, necrostatin-1, and YM155. We observed the growth inhibition of artesunate on HCT116 colon cancer cells by morphologic findings. Inhibition of cell growth was assessed by MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide) assay and long-term growth inhibition by colony-forming assay. Apoptosis was investigated by flow cytometry and Western blot analysis.
Results: Artesunate inhibited the proliferation of HCT116 colon cancer cells effectively. Co-treatment with YM155, a specific survivin inhibitor, enhanced the artesunate-induced cell death. Co-treatment with the iron-chelating agent deferoxamine rescued artesunate induced cell death and increased long-term cell survival and proliferation.
Conclusion: In this study, we demonstrated that artesunate-induced cytotoxicity in HCT116 colon cancer cells by suppressing the expression of survivin and partially by ferroptosis. Our findings suggest that the co-treatment artesunate with YM155 can induce more potent cell death on HCT116 colon cancer cells and shows new insight for the treatment of colorectal cancer patients.
Methods: We treated HCT116 colon cancer cells with artesunate, holo-transferrin, deferoxamine mesylate, ferrostatin, necrostatin-1, and YM155. We observed the growth inhibition of artesunate on HCT116 colon cancer cells by morphologic findings. Inhibition of cell growth was assessed by MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide) assay and long-term growth inhibition by colony-forming assay. Apoptosis was investigated by flow cytometry and Western blot analysis.
Results: Artesunate inhibited the proliferation of HCT116 colon cancer cells effectively. Co-treatment with YM155, a specific survivin inhibitor, enhanced the artesunate-induced cell death. Co-treatment with the iron-chelating agent deferoxamine rescued artesunate induced cell death and increased long-term cell survival and proliferation.
Conclusion: In this study, we demonstrated that artesunate-induced cytotoxicity in HCT116 colon cancer cells by suppressing the expression of survivin and partially by ferroptosis. Our findings suggest that the co-treatment artesunate with YM155 can induce more potent cell death on HCT116 colon cancer cells and shows new insight for the treatment of colorectal cancer patients.
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
참고문헌 (26)
참고문헌 신청
정규원 / 2017 / Cancer Statistics in Korea: Incidence, Mortality, Survival, and Prevalence in 2014 / Cancer Research and Treatment 49(2):292~305
Higgins CF / 2007 / Multiple molecular mechanisms for multidrug resistance transporters / Nature 446:749~757
Klayman DL / 1985 / Qinghaosu(artemisinin) : an antimalarial drug from China / Science 228:1049~1055
Pandey AV / 1999 / Artemisinin, an endoperoxide antimalarial, disrupts the hemoglobin catabolism and heme detoxification systems in malarial parasite / J Biol Chem 274:19383~19388
Kwok JC / 2002 / The iron metabolism of neoplastic cells : alterations that facilitate proliferation / Crit Rev Oncol Hematol 42:65~78
Higgins CF / 2007 / Multiple molecular mechanisms for multidrug resistance transporters / Nature 446:749~757
Klayman DL / 1985 / Qinghaosu(artemisinin) : an antimalarial drug from China / Science 228:1049~1055
Pandey AV / 1999 / Artemisinin, an endoperoxide antimalarial, disrupts the hemoglobin catabolism and heme detoxification systems in malarial parasite / J Biol Chem 274:19383~19388
Kwok JC / 2002 / The iron metabolism of neoplastic cells : alterations that facilitate proliferation / Crit Rev Oncol Hematol 42:65~78
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