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RISS 인기검색어
- 검색키워드
- 저자 : Jung Mungyo (검색결과 4 건)
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Senescent cancer cell-derived nanovesicle as a personalized therapeutic cancer vaccine
Hong Jihye,Jung Mungyo,Kim Cheesue,Kang Mikyung,Go Seokhyeong,Sohn Heesu,Moon Sangjun,Kwon Sungpil,Song Seuk Young,Kim Byung-Soo 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
The development of therapeutic cancer vaccines (TCVs) that provide clinical benefits is challenging mainly due to difficulties in identifying immunogenic tumor antigens and effectively inducing antitumor immunity. Furthermore, there is an urgent need for personalized TCVs because only a limited number of tumor antigens are shared among cancer patients. Several autologous nanovaccines that do not require the identification of immunogenic tumor antigens have been proposed as personalized TCVs. However, these nanovaccines generally require exogenous adjuvants (e.g., Toll-like receptor agonists) to improve vaccine immunogenicity, which raises safety concerns. Here, we present senescent cancer cell-derived nanovesicle (SCCNV) as a personalized TCV that provides patient-specific tumor antigens and improved vaccine immunogenicity without the use of exogenous adjuvants. SCCNVs are prepared by inducing senescence in cancer cells ex vivo and subsequently extruding the senescent cancer cells through nanoporous membranes. In the clinical setting, SCCNVs can be prepared from autologous cancer cells from the blood of liquid tumor patients or from tumors surgically removed from solid cancer patients. SCCNVs also contain interferon-γ and tumor necrosis factor-α, which are expressed during senescence. These endogenous cytokines act as adjuvants and enhance vaccine immunogenicity, avoiding the need for exogenous adjuvants. Intradermally injected SCCNVs effectively activate dendritic cells and tumor-specific T cells and inhibit primary and metastatic tumor growth and tumor recurrence. SCCNV therapy showed an efficacy similar to that of immune checkpoint blockade (ICB) therapy and synergized with ICB. SCCNVs, which can be prepared using a simple and facile procedure, show potential as personalized TCVs.
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The Senolytic Drug JQ1 Removes Senescent Cells via Ferroptosis
Seokhyeong GO,Mikyung KANG,Sung Pil KWON,Mungyo JUNG,Ok Hee JEON,Byung?Soo KIM 한국생물공학회 2021 한국생물공학회 학술대회 Vol.2021 No.10
Ferroptosis is an iron-dependent, non-apoptotic programmed cell death. Cellular senescence contributes to aging and various age-related diseases through the expression of a senescence-associated secretory phenotype (SASP). Senescent cells are often resistant to ferroptosis via increased ferritin and impaired ferritinophagy. In this study, we investigated whether treatment with JQ1 could remove senescent cells by inducing ferroptosis. We treated bleomycin-indueced senescent human dermal fibroblasts(HDFs) with JQ1 and determined whether JQ1 has senolytic effects with ferroptosis. At a certain range of JQ1 concentrations, JQ1 treatment reduced the viability and decreased SASP expression of senescent cells but did not reduce that of non-senescent cells, indicating that JQ1 treatment can selectively eliminate senescent cells. Subsequently, JQ1 treatment reduced the expression of ferroptosis-resistance genes and induced lipid peroxidation only in senescent cells. It suggested ferroptosis occurred in JQ1’s senolytic pathway. So, these data indicate that JQ1 can eliminate senescent cells via ferroptosis. This study suggests ferroptosis as a new mechanism of senolytic therapy.
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Kim, Na Kyung,Cha, Eun Jung,Jung, Mungyo,Kim, Jinseok,Jeong, Gun-Jae,Kim, Yong Seok,Choi, Woo Jin,Kim, Byung-Soo,Kim, Dong-Gyun,Lee, Jong-Chan The Royal Society of Chemistry 2019 Journal of materials chemistry. B, Materials for b Vol.7 No.21
<P>A mechanically tissue-like, biocompatible vitrimer film for tissue engineering scaffold applications is presented. 3D hierarchical scaffolds are prepared from the 2D vitrimer film <I>via</I> transesterification-induced hot embossing patterning and additional reconfiguration processes. Microsized grooves patterned on the vitrimer surface are found to enhance C2C12 cell elongation and alignment for promoted muscle regeneration.</P>
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Choo, Yeon Woong,Kang, Mikyung,Kim, Han Young,Han, Jin,Kang, Seokyung,Lee, Ju-Ro,Jeong, Gun-Jae,Kwon, Sung Pil,Song, Seuk Young,Go, Seokhyeong,Jung, Mungyo,Hong, Jihye,Kim, Byung-Soo American Chemical Society 2018 ACS NANO Vol.12 No.9
<P>Cancer immunotherapy modulates immune cells to induce antitumor immune responses. Tumors employ immune checkpoints to evade immune cell attacks. Immune checkpoint inhibitors such as anti-PD-L1 antibody (aPD-L1), which is being used clinically for cancer treatments, can block immune checkpoints so that the immune system can attack tumors. However, immune checkpoint inhibitor therapy may be hampered by polarization of macrophages within the tumor microenvironment (TME) into M2 tumor-associated macrophages (TAMs), which suppress antitumor immune responses and promote tumor growth by releasing anti-inflammatory cytokines and angiogenic factors. In this study, we used exosome-mimetic nanovesicles derived from M1 macrophages (M1NVs) to repolarize M2 TAMs to M1 macrophages that release pro-inflammatory cytokines and induce antitumor immune responses and investigated whether the macrophage repolarization can potentiate the anticancer efficacy of aPD-L1. M1NV treatment induced successful polarization of M2 macrophages to M1 macrophages <I>in vitro</I> and <I>in vivo</I>. Intravenous injection of M1NVs into tumor-bearing mice suppressed tumor growth. Importantly, injection of a combination of M1NVs and aPD-L1 further reduced the tumor size, compared to the injection of either M1NVs or aPD-L1 alone. Thus, our study indicates that M1NV injection can repolarize M2 TAMs to M1 macrophages and potentiate antitumor efficacy of the checkpoint inhibitor therapy.</P> [FIG OMISSION]</BR>
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