Mi Sun Park
The Breast Cancer Research Foundation
22 Papers
74 Citations
Mi Sun Park is an academic researcher from The Breast Cancer Research Foundation. The author has contributed to research in topics: Protein kinase B & PI3K/AKT/mTOR pathway. The author has an hindex of 10, co-authored 21 publications. Previous affiliations of Mi Sun Park include Seoul National University Hospital.
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Papers
Anti-apoptotic protein TCTP controls the stability of the tumor suppressor p53
Seung Bae Rho,Jeong Heon Lee,Mi Sun Park,Hyun-Jung Byun,Sokbom Kang,Sang-Soo Seo,Joo-Young Kim,Sang Yoon Park +7 more
TL;DR: TCTP physically interacts with p53 by interacting with anti tag coimmunoprecipitation by two hybrid TCTP particles.
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A series of novel terpyridine-skeleton molecule derivants inhibit tumor growth and metastasis by targeting topoisomerases.
Han Byeol Kwon,Chanmi Park,Kyung Hwa Jeon,Eunyoung Lee,So Eun Park,Kyu Yeon Jun,Tara Man Kadayat,Pritam Thapa,Radha Karki,Younghwa Na,Mi Sun Park,Seung Bae Rho,Eung-Seok Lee,Youngjoo Kwon +13 more
TL;DR: The modification of compounds 8 and 22 with the introduction of a methoxy instead of a hydroxy group enhanced endogenous topo inhibitory activity, metabolic stability in diverse types of liver microsomes and improved pharmacokinetic parameters in rat plasma such as augmentation of bioavailability.
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Thioridazine inhibits angiogenesis and tumor growth by targeting the VEGFR-2/PI3K/mTOR pathway in ovarian cancer xenografts
Mi Sun Park,Seung Myung Dong,Boh-Ram Kim,Seung Hee Seo,Sokbom Kang,Eun-Ju Lee,Seung-Hoon Lee,Seung Bae Rho +7 more
TL;DR: It is suggested that thioridazine might be a novel anti-tumor and anti-angiogenic agent for use in ovarian cancer through its role in regulating endothelial cell function and subsequent angiogenesis.
Anti-angiogenic effects of thioridazine involving the FAK-mTOR pathway.
Hyun-Jung Byun,Jeong Heon Lee,Boh-Ram Kim,Sokbom Kang,Seung Myung Dong,Mi Sun Park,Seung-Hoon Lee,Sung Ho Park,Seung Bae Rho +8 more
TL;DR: Evidence is provided for the regulation of endothelial cell functions that are relevant to angiogenesis through the suppression of the αvβ3/FAK/mTOR signaling pathway through the manipulation of the signaling regulators downstream of the focal adhesion kinase (FAK).
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sMEK1 inhibits endothelial cell proliferation by attenuating VEGFR-2-dependent-Akt/eNOS/HIF-1α signaling pathways.
TL;DR: It is suggested that sMEK1 might be a novel anti-angiogenic and anti-tumor agent for use in ovarian tumor by suppressing VEGFR-2-mediated PI3K/Akt/eNOS signaling pathway.