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Sook Kyung Park

Researcher at University of Texas at Austin

Publications -  9
Citations -  354

Sook Kyung Park is an academic researcher from University of Texas at Austin. The author has contributed to research in topics: Apoptosis & Downregulation and upregulation. The author has an hindex of 7, co-authored 7 publications receiving 329 citations.

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Tocotrienols induce apoptosis in breast cancer cell lines via an endoplasmic reticulum stress-dependent increase in extrinsic death receptor signaling

TL;DR: Results suggest that upregulation of DR5 by γ-T3 treatment is dependent on JNK and p38 MAPK activation which is mediated by ER-stress, and taken together, these results suggest that the anti-proliferative effects of tocotrienols were highly correlated with an increase in apoptosis based on Annexin V assessment.
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Role of Endoplasmic Reticulum Stress in α-TEA Mediated TRAIL/DR5 Death Receptor Dependent Apoptosis

TL;DR: ER stress plays an important role in α-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-ap optotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/ caspase -8 signaling.
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Anticancer actions of natural and synthetic vitamin E forms: RRR-α-tocopherol blocks the anticancer actions of γ-tocopherol

TL;DR: Both gammaT and alpha-TEA exhibited promising anticancer properties in vivo and in vitro, whereas all-rac-alphaT exhibited promising anti-cancer properties in vitro only, while alphaT not only failed to exhibit anticancers properties but it also reduced anticancer actions of gammaT in vivo.
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In vitro and in vivo evaluation of anticancer actions of natural and synthetic vitamin E forms.

TL;DR: Investigation of the potential anticancer properties of vitamin E in breast cancer models showed that synthetic, but not natural, vitamin E exhibits promising anti-cancer properties in vivo.
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α-TEA induces apoptosis of human breast cancer cells via activation of TRAIL/DR5 death receptor pathway.

TL;DR: These studies show that α‐TEA induces TRAIL/DR5 mitochondria‐dependent apoptosis in human breast cancer cells, and that TRAIL /DR5‐dependent increases in DR5 and decreases in c‐FLIP expression are triggered by TRAIL or α‐ TEA treatments.