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논문 기본 정보

자료유형
학술저널
저자정보
Shen Lei (Aerospace Center Hospital Beijing 100049 P.R. China) Lee Soon (Division of Analytical Science Korea Basic Science Institute Daejeon 34133 Republic of KoreaDivisio) Joo Jong Cheon (Department of Sasang Constitutional Medicine College of Korean Medicine Wonkwang University Iksan 5) Hong Eunmi (Division of Analytical Science Korea Basic Science Institute Daejeon 34133 Republic of Korea) Cui Zhen Yang (Rehabilitation Medicine College Weifang Medical University Weifang 261042 P.R. China) Jo Eunbi (Department of Life Science and Research Institute for Natural Sciences College of Natural Sciences) 박수정 (Department of Sasang Constitutional Medicine College of Korean Medicine Woosuk University Jeonju 54) 장현진 (Laboratory of Chemical Biology and Genomics Korea Research Institute of Bioscience and Biotechnolog)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제32권 제4호
발행연도
2022.4
수록면
493 - 503 (11page)
DOI
10.4014/jmb.2109.09030

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Forkhead transcription factor 3a (Foxo3a) is believed to be a tumor suppressor as its inactivation leads to cell transformation and tumor development. However, further investigation is required regarding the involvement of the activating transcription factor 3 (ATF3)-mediated Tat-interactive protein 60 (Tip60)/Foxo3a pathway in cancer cell apoptosis. This study demonstrated that Chelidonium majus upregulated the expression of ATF3 and Tip60 and promoted Foxo3a nuclear translocation, ultimately increasing the level of Bcl-2-associated X protein (Bax) protein. ATF3 overexpression stimulated Tip60 expression, while ATF3 inhibition by siRNA repressed Tip60 expression. Furthermore, siRNA-mediated Tip60 inhibition significantly promoted Foxo3a phosphorylation, leading to blockade of Foxo3a translocation into the nucleus. Thus, we were able to deduce that ATF3 mediates the regulation of Foxo3a by Tip60. Moreover, siRNA-mediated Foxo3a inhibition suppressed the expression of Bax and subsequent apoptosis. Taken together, our data demonstrate that Chelidonium majus induces SKOV-3 cell death by increasing ATF3 levels and its downstream proteins Tip60 and Foxo3a. This suggests a potential therapeutic role of Chelidonium majus against ovarian cancer.

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