81 research outputs found
Abstract 4310: SH003 induces apoptosis of DU145 prostate cancer cells by inhibiting ERK-involved pathway
No full textAbstract
Herbal medicines have been used in cancer treatment, with many exhibiting favorable side effect and toxicity profiles compared with conventional chemotherapeutic agents. SH003 is a novel extract from Astragalus membranaceus, Angelica gigas, and Trichosanthes Kirilowii Maximowicz combined at a 1:1:1 ratio that impairs the growth of breast cancer cells. Our data demonstrate that SH003 induced apoptosis in DU145 prostate cancer cells by inhibiting ERK signaling. SH003 induced apoptosis of prostate cancer cells in dose-dependent manner, which was independent of androgen dependency. SH003 also increased intracellular ROS levels but this is not associated with its pro-apoptotic effects. SH003 inhibited phosphorylation of Ras/Raf1/MEK/ERK/p90RSK in androgen-independent DU145 cells, but not androgen-dependent LNCaP and PC-3 cells. Moreover, ERK2 overexpression rescued SH003-induced apoptosis in DU145 cells. Thus, our data conclude that SH003 induces apoptotic cell death of DU145 prostate cancer cells by inhibiting ERK-mediated pathway.
Citation Format: Yu-Jeong Choi, Myeong-Sun Kim, Soo-Yeon Kang, Kangwook Lee, Jin Mo Ku, Se Hyang Hong, Hyo In Kim, Chunhoo Cheon, Youme Ko, Huang Ching Wen, Yui Sasaki, Sohyeon Kang, Tai Young Kim, Ji Hye Kim, Yong Cheol Shin, Seong-Gyu Ko. SH003 induces apoptosis of DU145 prostate cancer cells by inhibiting ERK-involved pathway [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4310. doi:10.1158/1538-7445.AM2017-4310</jats:p
Disorder-induced electronic, magnetic, and optoelectronic properties of two-dimensional materials
No full textTechnological advancement has been in cadence with material development by improving the purity of single crystals and, at the same time, controlling their imperfections. These capabilities have been especially vital for developing new technolo-gies based on two-dimensional (2D) van der Waals (vdW) materials for future electronic and optoelectronic applications. This is because the inherent properties of 2D vdW materials is highly susceptible to the presence of intrinsic structural defects and ex-trinsic disorders due to large surface-area-to-volume ratio. The successful reduction of these disorders has significantly im-proved material properties and led to the discovery of novel physical phenomena in vdW materials. On the other hand, structural defects â for instance, 0-dimensional point defects â can induce completely new properties that are otherwise absent in the pre-fect lattice. To harness the full potential of vdW materials, it is thus essential to produce high-quality crystals and understand how the disorder affects their material properties, which is the central idea of this dissertation.
In this dissertation, we first present the work of high-quality epitaxial growth of NbS2. Based on atmospheric-pressure chemical vapor deposition, we have successfully synthesized the two polymorphs (2H and 3R) of NbS2 with the largest lateral size grown to date. Their distinct superconducting and metallic properties were examined under low-temperature charge transport, respectively. Our finding demonstrates the practical synthesis method for phase-controllable growth of 2D transition metal dichalcogenides and can benefit future studies in mesoscopic devices and large-area applications of 2D superconductors.
Secondly, we present the work of discovering defect-induced novel properties in ultrathin layers of PtSe2. Although bulk PtSe2 is non-magnetic, we observe the appearance of magnetism in monolayer and bilayer PtSe2. We were able to measure the magnetoresistance (MR) of mono- and bilayer PtSe2 under perpendicular magnetic fields using proximitized graphene, and found antiferromagnetic and ferromagnetic MR responses for mono- and bilayer, respectively. The appearance of such different magnetic states is theoretically explained by the first-principle density functional theory calculation, suggesting the origin of induced-magnetic moments from intrinsic Pt vacancies for both layers. Moreover, we also found that structural disorder in PtSe2 can induce bulk photovoltaic effect (BPVE). The second-order optical nonlinear effects, such as BPVE, require broken structural inversion symmetry and crystal symmetry can be reduced by the presence of structural defects. The broken local inversion symmetry from structural disorder in centrosymmetric PtSe2 is manifested by the generation of zero-biased photo-current under homogenous illumination. We observe linear and circular polarization-dependent photocurrents in defective PtSe2, which is largely absent in the pristine crystal. Our findings in PtSe2 emphasize the importance of the structural disorder for generating completely new properties and stress the need for defect-engineering for realizing the practical use of PtSe2 in spintronic and photovoltaic applications.LANE
Abstract 300: Taeumjowi-tang (TJ001) induces G2/M cell cycle arrest but not apoptosis in p53-mutant prostate cancer via up-regulation of p21WAF/CIP1
No full textAbstract
Taeumjowi-tang (TJ001) is a traditional Korean medicine that usually prescribed for Tae-um person to regulate stomach-related symptoms including headache, indigestion, and jaundice. Other studies on anti-obesity effect of TJ001 have also been researched, but have never been reported as a cure for cancer. In the present study, we investigated the molecular mechanism that TJ001 induces G2/M cell cycle arrest in DU145 (p53-mutant) prostate cancer cells. The missense mutation in human p53 gene (TP53) confers oncological effect to tumor suppressor p53-mutant protein. In prostate cancer, this gain-of-function of p53-mutant is associated with androgen-independence, increased angiogenesis, and metastasis. Our in vitro studies showed that a water extract of TJ001 induced G2/M cell cycle arrest via p53-mutant status and p21WAF/CIP1 up-regulation. Conventinally, p21WAF/CIP1 is induced by mediating p53 regulation, but, in experiments, handling the p53-dependent and -independent pathway. Although serine15-phosphorylated p53 and p53 proteins remained unchanged, p21WAF/CIP1 expression is induced and cyclin B1/Cdc2 complex is inactivated by a decrease of cyclin B1. In addition, in p53-independent pathway, the level of Cdc25C expression decreased and Serine-216 phosphorylated Cdc25C increased. Generally, concomitant with G2/M cell cycle arrest come the apoptosis cell death, but in the study, prolonged G2/M cell cycle arrest developed not apoptosis but cell senescence. Therefore, our data suggest that TJ001 is helpful for p53-mutant prostate cancer treatment.
Citation Format: Soo-Yeon Kang, Hyo In Kim, Se Hyang Hong, Jin Mo Ku, Kangwook Lee, Myeong-Sun Kim, Yu-jeong Choi, Chunhoo Cheon, Youme Ko, Ching Wen Huang, Yui Sasaki, Sohyeon Kang, Hye-Sook Seo, Tai Young Kim, Ji Hye Kim, Yong Cheol Shin, Seong-Gyu Ko. Taeumjowi-tang (TJ001) induces G2/M cell cycle arrest but not apoptosis in p53-mutant prostate cancer via up-regulation of p21WAF/CIP1 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 300. doi:10.1158/1538-7445.AM2017-300</jats:p
Abstract 2320: Cucurbitacin D induces cell cycle arrest and apoptosis by inhibiting STAT3 and NF-κB signaling in doxorubicin-resistant human breast carcinoma (MCF7/ADR) cells
No full textAbstract
Objective: We examined whether cucurbitacin D affects doxorubicin resistance of MCF7/ADR breast cancer cells.
Methods: Cell viability was measured by MTT assay. Levels of p-STAT3, p-NF-κB, IκB, and caspases were measured by western blot analysis. Nuclear staining of Stat3 and NF-κB was measured by immunocytochemistry. STAT3 and NF-κB transcriptional activity was detected by STAT3 and NF-κB luciferase reporter gene assays. Analysis of cell cycle arrest was performed by flow cytometry. Induction of apoptosis by cucurbitacin D was measured by annexin VFITC/PI assay.
Results: More than 90% of MCF7/ADR cells lived upon treatment with doxorubicin for 24 h. However, upon treatment with cucurbitacin D, cell death was more than 60%. Co-administration of cucurbitacin D and doxorubicin induced apoptosis, G2/M cell cycle arrest, and inhibited upregulated Stat3 by doxorubicin on MCF7/ADR cells. Additionally, cucurbitacin D led to an increase in the IκBα level in the cytosol and a decrease in the p-NF-κB level in the nucleus. Finally, cucurbitacin D inhibited translocation of Stat3 and NF-κB and decreased transcriptional activity in the nucleus.
Conclusion: Cucurbitacin D decreases cell proliferation and induces apoptosis by inhibiting Stat3 and NF-κB signaling in doxorubicin-resistant breast cancer cells. Cucurbitacin D could be used as a useful compound to treat Adriamycin-resistant patients.
Note: This abstract was not presented at the meeting.
Citation Format: Jin Mo Ku, Se Hyang Hong, Myeong-Sun Kim, Hyo In Kim, Soo-Yeon Kang, Kangwook Lee, Yu-Jeong Choi, Chunhoo Cheon, CHING WEN HUANG, Youme Ko, Yui Sasaki, Sohyeon Kang, Ji Hye Kim, Hye Sook Seo, Tai Young Kim, Yong Cheol Shin, Seong-Gyu Ko. Cucurbitacin D induces cell cycle arrest and apoptosis by inhibiting STAT3 and NF-κB signaling in doxorubicin-resistant human breast carcinoma (MCF7/ADR) cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2320. doi:10.1158/1538-7445.AM2017-2320</jats:p
Abstract 4010: Tonggyu-tang, a traditional Korean medicine, suppresses inflammation, potential implications in tumor microenvironment
No full textAbstract
The critical roles of inflammation in the development of cancer have long been appreciated. A growing body of evidence supports the notion that infiltrates of inflammatory cells into tumor microenvironment influence the tumor progression by providing bioactive molecules including pro-inflammatory cytokines. Importantly, the increased number of mast cells within tumor microenvironment has been associated with a poor survival in cancer patients. Moreover, keratinocyte inflammation is known to be crucial for skin tumor development. The use of natural products to reduce inflammation in tumor microenvironment is gaining an interest, because of their reduced toxicity toward normal cells. In this study, we tested the effects of Tonggyu-tang (TGT) which is composed of 14 different herbal extracts on the activity of mast cells. We found that TGT significantly reduced the expression and production of inflammatory cytokines such as IL-4, IL-6, IL-8, and TNF-α in PMA and ionomycin- stimulated HMC-1 (human mast cell line-1). In an attempt to determine molecular mechanism underlying the inhibitory effects of TGT on cytokine expression, we revealed that TGT suppressed MAPK signaling pathway including ERK, p38, and JNK as well as NF-κB pathway, which are known to regulate inflammatory cytokine expression. Similar results were obtained from the LPS-stimulated HaCaT cells, immortalized human keratinocytes. Taken together, our results demonstrate that TGT suppresses inflammation by inhibiting the expression of pro-inflammatory cytokine in both mast cells and keratinocytes, thereby potentially leading to inhibition of tumor progression.
Citation Format: Hyoin Kim, Seong-Gyu Ko, Yong Cheol Shin, Ji Hye Kim, Hye-Sook Seo, Tai Young Kim, Se Hyang Hong, Kangwook Lee, Jin Mo Ku, Myeong-Sun Kim, Yu-Jeong Choi, Soo-yeon Kang, Chunhoo Cheon, Youme Ko, Huang Ching Wen, Yui Sasaki, Sohyeon Kang. Tonggyu-tang, a traditional Korean medicine, suppresses inflammation, potential implications in tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4010. doi:10.1158/1538-7445.AM2017-4010</jats:p
ChemInform Abstract: Cyanide as a Powerful Catalyst for Facile Synthesis of Benzofused Heteroaromatic Compounds via Aerobic Oxidation.
No full textChemInform Abstract: Synthesis of 2‐Aminoquinoxalines via One‐Pot Cyanide‐Based Sequential Reaction under Aerobic Oxidation Conditions.
No full textScreening of the inhibitory activity of medicinal plants against VHR dual-specificity protein tyrosine phosphatase(DS-PTPase)
No full textThe methanol extracts of 162 herbal medicines were screened for the inhibitory activity against VHR dualspecificity protein tyrosine phosphatase (DS-PTPase). Seventeen medicinal plants, Scutellaria baicalensis, Cuscuta chinensis, Caesalpinia sappan, Arecae pericarpium, Rubus coreanus, Machilus thunbergii, Amsonia elliptica, Cinnamomum cassia, Arisaema erubescens, Pueraria thunbergiana, Dendrobium moniliforme, Mentha arvensis, Peucedanum japonicum, Salvia miltiorrhiza, Leonurus sibiricus, Siegesbeckia orientalis, Prunella vulgaris showed potent VHR DS-PTPase inhibitory activity.open
Distinctive Dynamics and Functions of the CD4+CD25+FOXP3+ Regulatory T Cell Population in Patients with Severe and Mild COVID-19
No full textAlthough CD4+CD25+FOXP3+ regulatory T (TREG) cells have been studied in patients with COVID-19, changes in the TREG cell population have not been longitudinally examined during the course of COVID-19. In this study, we longitudinally investigated the quantitative and qualitative changes in the TREG cell population in patients with COVID-19. We found that the frequencies of total TREG cells and CD45RA-FOXP3hi activated TREG cells were significantly increased 15-28 d postsymptom onset in severe patients, but not in mild patients. TREG cells from severe patients exhibited not only increased proliferation but also enhanced apoptosis, suggesting functional derangement of the TREG cell population during severe COVID-19. The suppressive functions of the TREG cell population did not differ between patients with severe versus mild COVID-19. The frequency of TREG cells inversely correlated with SARS-CoV-2-specific cytokine production by CD4+ T cells and their polyfunctionality in patients with mild disease, suggesting that TREG cells are major regulators of virus-specific CD4+ T cell responses during mild COVID-19. However, such correlations were not observed in patients with severe disease. Thus, in this study, we describe distinctive changes in the TREG cell population in patients with severe and mild COVID-19. Our study provides a deep understanding of host immune responses upon SARS-CoV-2 infection in regard to TREG cells. Copyright © 2023 by The American Association of Immunologists, Inc.11Nsciescopu
Corticosteroids reduce pathologic interferon responses by downregulating STAT1 in patients with high-risk COVID-19
No full textWe do not yet understand exactly how corticosteroids attenuate hyperinflammatory responses and alleviate high-risk coronavirus disease 2019 (COVID-19). We aimed to reveal the molecular mechanisms of hyperinflammation in COVID-19 and the anti-inflammatory effects of corticosteroids in patients with high-risk COVID-19. We performed single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from three independent COVID-19 cohorts: cohort 1 was used for comparative analysis of high-risk and low-risk COVID-19 (47 PBMC samples from 28 patients), cohort 2 for longitudinal analysis during COVID-19 (57 PBMC samples from 15 patients), and cohort 3 for investigating the effects of corticosteroid treatment in patients with high-risk COVID-19 (55 PBMC samples from 13 patients). PBMC samples from healthy donors (12 PBMC samples from 12 donors) were also included. Cohort 1 revealed a significant increase in the proportion of monocytes expressing the long noncoding RNAs NEAT1 and MALAT1 in high-risk patients. Cohort 2 showed that genes encoding inflammatory chemokines and their receptors were upregulated during aggravation, whereas genes related to angiogenesis were upregulated during improvement. Cohort 3 demonstrated downregulation of interferon-stimulated genes (ISGs), including STAT1, in monocytes after corticosteroid treatment. In particular, unphosphorylated STAT-dependent ISGs enriched in monocytes from lupus patients were selectively downregulated by corticosteroid treatment in patients with high-risk COVID-19. Corticosteroid treatment suppresses pathologic interferon responses in monocytes by downregulating STAT1 in patients with high-risk COVID-19. Our study provides insights into the mechanisms underlying COVID-19 aggravation and improvement and the effects of corticosteroid treatment. © 2023, The Author(s).11Nsciescopuskc
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