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Byun, Sanguine,Lim, Semi,Mun, Ji Young,Kim, Ki Hyun,Ramadhar, Timothy R.,Farrand, Lee,Shin, Seung Ho,Thimmegowda, N. R.,Lee, Hyong Joo,Frank, David A.,Clardy, Jon,Lee, Sam W.,Lee, Ki Won American Society for Biochemistry and Molecular Bi 2015 The Journal of biological chemistry Vol.290 No.39
<P>Bioactive phytochemicals can suppress the growth of malignant cells, and investigation of the mechanisms responsible can assist in the identification of novel therapeutic strategies for cancer therapy. Ginger has been reported to exhibit potent anti-cancer effects, although previous reports have often focused on a narrow range of specific compounds. Through a direct comparison of various ginger compounds, we determined that gingerenone A selectively kills cancer cells while exhibiting minimal toxicity toward normal cells. Kinase array screening revealed JAK2 and S6K1 as the molecular targets primarily responsible for gingerenone A-induced cancer cell death. The effect of gingerenone A was strongly associated with relative phosphorylation levels of JAK2 and S6K1, and administration of gingerenone A significantly suppressed tumor growth <I>in vivo</I>. More importantly, the combined inhibition of JAK2 and S6K1 by commercial inhibitors selectively induced apoptosis in cancer cells, whereas treatment with either agent alone did not. These findings provide rationale for dual targeting of JAK2 and S6K1 in cancer for a combinatorial therapeutic approach.</P>
Therapeutic Implications of Autophagy Inducers in Immunological Disorders, Infection, and Cancer
Byun, Sanguine,Lee, Eunjung,Lee, Ki Won MDPI AG 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.9
<P>Autophagy is an essential catabolic program that forms part of the stress response and enables cells to break down their own intracellular components within lysosomes for recycling. Accumulating evidence suggests that autophagy plays vital roles in determining pathological outcomes of immune responses and tumorigenesis. Autophagy regulates innate and adaptive immunity affecting the pathologies of infectious, inflammatory, and autoimmune diseases. In cancer, autophagy appears to play distinct roles depending on the context of the malignancy by either promoting or suppressing key determinants of cancer cell survival. This review covers recent developments in the understanding of autophagy and discusses potential therapeutic interventions that may alter the outcomes of certain diseases.</P>
Sanguine Byun 한국식품영양과학회 2021 한국식품영양과학회 학술대회발표집 Vol.2021 No.10
The importance of a diet high in fruits and vegetables has long been suspected to play a role in the prevention and treatment of various diseases. Observations from epidemiological studies of dietary patterns have stimulated interest in the field of natural products and functional food research, which aims to characterize compounds from natural sources that have health benefits beyond their normal nutritional properties. However, identifying potent bioactive food compounds can be a hurdle in developing novel functional foods. Therefore, we have applied high-throughput screening technology to compare the bioactivity of various food/natural compounds and to elucidate their molecular mechanism in an attempt to develop novel food materials with enhanced functionality. These findings will provide the rationale to utilize high-throughput screening technology in the field of functional food science.
Bae, Seong-Yeon,Byun, Sanguine,Bae, Soo Han,Min, Do Sik,Woo, Hyun Ae,Lee, Kyunglim Informa UK (TaylorFrancis) 2017 AUTOPHAGY Vol.13 No.5
<P>TPT1/TCTP (tumor protein, translationally-controlled 1) is highly expressed in tumor cells, known to participate in various cellular activities including protein synthesis, growth and cell survival. In addition, TPT1 was identified as a direct target of the tumor suppressor TP53/p53 although little is known about the mechanism underlying the anti-survival function of TPT1. Here, we describe a role of TPT1 in the regulation of the MTORC1 pathway through modulating the molecular machinery of macroautophagy/autophagy. TPT1 inhibition induced cellular autophagy via the MTORC1 and AMPK pathways, which are inhibited and activated, respectively, during treatment with the MTOR inhibitor rapamycin. We also found that the depletion of TPT1 potentiated rapamycin-induced autophagy by synergizing with MTORC1 inhibition. We further demonstrated that TPT1 knockdown altered the BECN1 interactome, a representative MTOR-independent pathway, to stimulate autophagosome formation, via downregulating BCL2 expression through activating MAPK8/JNK1, and thereby enhancing BECN1-phosphatidylinositol 3-kinase (PtdIns3K)-UVRAG complex formation. Furthermore, reduced TPT1 promoted autophagic flux by modulating not only early steps of autophagy but also autophagosome maturation. Consistent with in vitro findings, in vivo organ analysis using Tpt1 heterozygote knockout mice showed that autophagy is enhanced because of haploinsufficient TPT1 expression. Overall, our study demonstrated the novel role of TPT1 as a negative regulator of autophagy that may have potential use in manipulating various diseases associated with autophagic dysfunction.</P>
Farrand, Lee,Kim, Ji Young,Byun, Sanguine,Im-aram, Akechai,Lee, Jihoon,Suh, Jeong-Yong,Lee, Ki-Won,Lee, Hyong Joo,Tsang, Benjamin K. American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.3
<▼1><P><B>Background:</B> Resistance of ovarian cancer cells to chemotherapy is a major therapeutic problem.</P><P><B>Results:</B> Hirsutenone induces cisplatin sensitivity via p53, X-linked inhibitor of apoptosis protein, and apoptosis-inducing factor.</P><P><B>Conclusion:</B> Hirsutenone sensitizes resistant ovarian cancer cells to cisplatin.</P><P><B>Significance:</B> Co-treatment with hirsutenone may have the potential to overcome chemoresistance.</P></▼1><▼2><P>Cisplatin (CDDP) and its derivatives are considered first-line treatments for ovarian cancer (OVCA). However, despite initial results that often appear promising, in most cases patients will return with recurrent disease that fails to respond to further chemotherapy. We assayed a number of food phytochemicals with reported PI3K inhibitory ability to identify candidates that can influence CDDP treatment outcomes in chemoresistant OVCA cell lines. A direct comparison revealed that the diarylheptanoid hirsutenone from the tree bark of <I>Alnus hirsuta</I> var. sibirica was superior at inducing CDDP sensitivity in a number of chemoresistant cancer cell lines. Whereas hirsutenone treatment activated p53, its modest efficacy in <I>p53</I>-mutant and -null cell lines suggested the existence of a p53-independent mode of action. Further investigation revealed that hirsutenone causes CDDP-dependent apoptosis in chemoresistant cells by ubiquitin-proteasome-dependent X-linked inhibitor of apoptosis degradation and by enhancing the translocation of apoptosis-inducing factor from the mitochondria to the nucleus. This was found to be, at least in part, under the influence of upstream Akt activity, linking hirsutenone-dependent PI3K inhibition with downstream effects on apoptosis-inducing factor, X-linked inhibitor of apoptosis, and apoptosis. Our findings provide rationale for further investigation of the effects of hirsutenone on chemoresistant OVCA in clinical studies.</P></▼2>