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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
- 2024.12
- 수록면
- 209 - 218 (10page)
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초록· 키워드
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Objectives: Arctigenin, a lignan extracted from the greater burdock has been traditionally used as a medicinal herb. Breast cancer researchers use three markers to classify the type of breast cancer: estrogen receptor (ER), human epidermal growth factor receptor 2 (HER2), and progesterone receptor (PR). This study investigated the anticancer effects of arctigenin and its mechanisms of action in three breast cancer cell lines: MCF-7 (ER+/HER2+/PR–), SK-BR-3 (ER–/HER2+/PR–), and MDA-MB-231 (ER–/HER2–/PR–).
Methods: The anticancer efficacy was assessed using the WST cell viability assay, while the mechanisms of apoptosis induction were analyzed through Annexin V-FITC/PI staining and Western blotting.
Results: In our results, arctigenin at a concentration of less than 50 uM did not inhibit the growth of ER-positive MCF-7 cells.
In contrast, arctigenin at concentrations ranging from 0.39 to 50 uM inhibited the development of ER-negative cells, SK-BR-3 and MDA-MB-231. Western blot analysis and annexin V-FITC/PI analysis revealed that apoptosis was involved in the death of arctigenin-treated cancer cells. Specifically, it was observed that increased levels of cleaved PARP, cleaved caspase-3, and cleaved caspase-9, along with decreased levels of XIAP and Survivin, and an increased Bax/Bcl-2 ratio in arctigenin-treated SK-BR-3 and MDA-MB-231 cells.
Conclusion: These results indicated that arctigenin induced cell death by activating apoptosis in ER–/HER2+ SK-BR-3 and ER–/ HER2– MDA-MB-231 breast cancer cells. Consequently, these results support the potential use of arctigenin as a therapeutic agent for ER– breast cancer treatment.
Methods: The anticancer efficacy was assessed using the WST cell viability assay, while the mechanisms of apoptosis induction were analyzed through Annexin V-FITC/PI staining and Western blotting.
Results: In our results, arctigenin at a concentration of less than 50 uM did not inhibit the growth of ER-positive MCF-7 cells.
In contrast, arctigenin at concentrations ranging from 0.39 to 50 uM inhibited the development of ER-negative cells, SK-BR-3 and MDA-MB-231. Western blot analysis and annexin V-FITC/PI analysis revealed that apoptosis was involved in the death of arctigenin-treated cancer cells. Specifically, it was observed that increased levels of cleaved PARP, cleaved caspase-3, and cleaved caspase-9, along with decreased levels of XIAP and Survivin, and an increased Bax/Bcl-2 ratio in arctigenin-treated SK-BR-3 and MDA-MB-231 cells.
Conclusion: These results indicated that arctigenin induced cell death by activating apoptosis in ER–/HER2+ SK-BR-3 and ER–/ HER2– MDA-MB-231 breast cancer cells. Consequently, these results support the potential use of arctigenin as a therapeutic agent for ER– breast cancer treatment.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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