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Kyoung‑jin Min,Sk Abrar Shahriyar,권택규 한국독성학회 2020 Toxicological Research Vol.36 No.2
Arylquin 1, a small-molecule prostate-apoptosis-response-4 (Par-4) secretagogue, targets vimentin to induce Par-4 secretion. Secreted Par-4 binds to its receptor, 78-kDa glucose-regulated protein (GRP78), on the cancer cell surface and induces apoptosis. In the present study, we investigated the molecular mechanisms of arylquin 1 in cancer cell death. Arylquin 1 induces morphological changes (cell body shrinkage and cell detachment) and decreases cell viability in various cancer cells. Arylquin 1-induced cell death is not inhibited by apoptosis inhibitors (z-VAD-fmk, a pan-caspase inhibitor), necroptosis inhibitors (necrostatin-1), and paraptosis inhibitors. Furthermore, arylquin 1 significantly induces reactive oxygen species levels, but antioxidants [N-acetyl-l-cysteine and glutathione ethyl ester] do not inhibit arylquin 1-induced cell death. Furthermore, Par-4 knock-down by small interfering RNA confers no effect on cytotoxicity in arylquin 1-treated cells. Interestingly, arylquin 1 induces lysosomal membrane permeabilization (LMP), and cathepsin inhibitors and overexpression of 70-kDa heat shock protein (HSP70) markedly prevent arylquin 1-induced cell death. Therefore, our results suggest that arylquin 1 induces non-apoptotic cell death in cancer cells through the induction of LMP.
Elucidation for modulation of death receptor (DR) 5 to strengthen apoptotic signals in cancer cells
Kyoung-jin Min,Seon Min Woo,Sk Abrar Shahriyar,Taeg Kyu Kwon 대한약학회 2019 Archives of Pharmacal Research Vol.42 No.1
The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis via death receptor (DR) 4 or DR5 preferentially in cancer cells, and not in normal cells with relatively high decoy receptor expression. However, multiple mechanisms in cancer cells induce resistance to DRs-mediated apoptosis. Therefore, understanding of molecular mechanisms for resistance to DRs-mediated apoptosis can find the strategy to increase sensitivity. Although multiple proteins are involved in resistance to DRs-mediated apoptosis, we focus on modulation of DR5 to overcome resistance. Here, we discuss regulation of DR5 expression or activation by epigenetic modification, transcription factor at the transcriptional levels, micro RNA and RNA-binding proteins at the posttranscriptional levels, and ubiquitination and glycosylation at the post-translational levels. In addition, we also mention about relationship between localization of DR5 and death signaling activation. The purpose of this review is to help understand relationship between regulatory mechanisms of DR5 and resistance to TRAIL or DRs-targeted agonist monoclonal antibodies, and to develop innovative anticancer therapies through regulation of DR5 signaling.
항암화학요법을 받은 부인암 환자의 혈액학적 분석을 통한 임상적 고찰
이선경,김승보,김선호,김응선,진규섭,이보연,허주엽 대한부인종양 콜포스코피학회 1997 Journal of Gynecologic Oncology Vol.8 No.3
Anticancer chemotherapy has important role in gynecologic cancer treatment and the use of combination chemotherapy in which two or more drugs are combined, has been increased. 64 gynecologic cancer patients who treated with combination anticancer chemotherapy were reviewed retrospectively in this study for the evaluation of drug toxicity by using hematologic monitoring. The results were as follows: 1. Leukocyte count was the most important parameter in the bone marrow toxicity. And granulocyte and platelet count must by monitored if leukocytopenia is developed. 2. Considering the severe drug toxicity over grade 3, leukopenia in VBP(Vinblastine, Bleomycin, Cis-platin), CAP(Cyclophospamide, Adriamycin, Cis-platin), CDDP-5FU(Cis-platin, 5-Fluorouracil) were 8 cases(32%), 3 cases(23%), and 3 cases(20%) respectively. And severe thrombocytopenia in VBP, CAP, and CDDP-5FU were 2 cases(7%), 1 cases(8%), and 1 cases(6%) respectively. Severe anemia was 3 cases(23%) in CAP, and hepatotoxicity was 1 cases(14%) in CP(Cyclophosphamide, Cis-platin) chemotherapy. 3. Concerning the VBP, CAP and CDDP-5FU regimen, there was no significant correlation between the number of cycle and the changes of hematologic variables especially leukocyte and platelet count. So it is difficult to predict the time of severe myelosuppression with hematologic evaluation alone. Follow up hematologic monitoring with regular interval may be useful for the early detection of myelosuppression.
Ahmed, Sk. Faruque,Yi, Jin Woo,Moon, Myoung-Woon,Jang, Yong-Jun,Park, Bong-Hyun,Lee, Seong-Hoon,Lee, Kwang-Ryeol WILEY-VCH Verlag 2009 Plasma Processes and Polymers Vol.6 No.12
<P>This study examined the surface morphological evolution of polycarbonate and acrylonitrile butadiene styrene (PC/ABS) irradiated with an Ar ion beam using an ion beam system. PC was not affected by the Ar ion beam treatment at a lower ion beam treatment times but the ABS portion formed a foam-like nanostructure at the surface. On the other hand, both PC and ABS formed nanostructures with length of 100 to 120 nm and a mean diameter of ≈35 nm at longer beam treatment times. The Raman and FTIR spectra revealed polymer chain scissioning. Nanoindentation showed that the hardness and elastic modulus of the PC/ABS decreases from 0.22 to 0.18 GPa and from 3.39 to 2.98 GPa, respectively with increasing Ar ion beam treatment time due to the surface nano-structures formed by Ar ion beam.</P><P> <img src='wiley_img/16128850-2009-6-12-PPAP200900043-gra001.gif' alt='wiley_img/16128850-2009-6-12-PPAP200900043-gra001'> </P> <B>Graphic Abstract</B> <P>The surface morphological evolution of PC/ABS irradiated with an Ar ion beam using an ion beam system has been studied. PC was not affected by the Ar ion beam treatment at a lower ion beam treatment times but the ABS portion formed a foam-like nanostructure at the surface induced by polymer chain scissioning. As increase the treatment times, both PC and ABS formed nanostructures with length of 100 to 120nm and a mean diameter of ≈35nm. <img src='wiley_img/16128850-2009-6-12-PPAP200900043-content.gif' alt='wiley_img/16128850-2009-6-12-PPAP200900043-content'> </P>
Shahriyar, Sk Abrar,Woo, Seon Min,Seo, Seung Un,Min, Kyoung-jin,Kwon, Taeg Kyu MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.10
<P>Cepharanthine (CEP) is a natural plant alkaloid, and has anti-inflammatory, antineoplastic, antioxidative and anticancer properties. In this study, we investigated whether CEP could sensitize renal carcinoma Caki cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. CEP alone and TRAIL alone had no effect on apoptosis. However, combined CEP and TRAIL treatment markedly enhanced apoptotic cell death in cancer cells, but not in normal cells. CEP induced downregulation of survivin and cellular-FLICE inhibitory protein (c-FLIP) expression at post-translational levels. Ectopic expression of survivin blocked apoptosis by combined treatment with CEP plus TRAIL, but not in c-FLIP overexpression. Interestingly, CEP induced survivin downregulation through downregulation of deubiquitin protein of STAM-binding protein-like 1 (STAMBPL1). Overexpression of STAMBPL1 markedly recovered CEP-mediated survivin downregulation. Taken together, our study suggests that CEP sensitizes TRAIL-mediated apoptosis through downregulation of survivin expression at the post-translational levels in renal carcinoma cells.</P>