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Calnexin as a dual-role biomarker: antibody-based diagnosis and therapeutic targeting in lung cancer
( Soyeon Lim ),( Youngeun Ha ),( Boram Lee ),( Junho Shin ),( Taiyoun Rhim ) 생화학분자생물학회 2024 BMB Reports Vol.57 No.3
Lung cancer carries one of the highest mortality rates among all cancers. It is often diagnosed at more advanced stages with limited treatment options compared to other malignancies. This study focuses on calnexin as a potential biomarker for diagnosis and treatment of lung cancer. Calnexin, a molecular chaperone integral to N-linked glycoprotein synthesis, has shown some associations with cancer. However, targeted therapeutic or diagnostic methods using calnexin have been proposed. Through 1D-LCMSMS, we identified calnexin as a biomarker for lung cancer and substantiated its expression in human lung cancer cell membranes using Western blotting, flow cytometry, and immunocytochemistry. Anti-calnexin antibodies exhibited complement-dependent cytotoxicity to lung cancer cell lines, resulting in a notable reduction in tumor growth in a subcutaneous xenograft model. Additionally, we verified the feasibility of labeling tumors through in vivo imaging using antibodies against calnexin. Furthermore, exosomal detection of calnexin suggested the potential utility of liquid biopsy for diagnostic purposes. In conclusion, this study establishes calnexin as a promising target for antibody-based lung cancer diagnosis and therapy, unlocking novel avenues for early detection and treatment.
Enhanced Calreticulin Expression Promotes Calcium-dependent Apoptosis in Postnatal Cardiomyocytes
Lim, Soyeon,Chang, Woochul,Lee, Byoung Kwon,Song, Heesang,Hong, Ja Hyun,Lee, Sunju,Song, Byeong Wook,Kim, Hye Jung,Cha, Min Ji,Jang, Yangsoo,Chung, Namsik,Choi, Soon Yong,Hwang, Ki Chul Korean Society for Molecular Biology 2008 Molecules and cells Vol.25 No.3
Calreticulin (CRT) is one of the major Ca<SUP>2+</SUP> binding chaperone proteins of the endoplasmic reticulum (ER) and an unusual luminal ER protein. Postnatally elevated expression of CRT leads to impaired development of the cardiac conductive system and may be responsible for the pathology of complete heart block. In this study, the molecular mechanisms that affect Ca2+-dependent signal cascades were investigated using CRT-overexpressing cardiomyocytes. In particular, we asked whether calreticulin plays a critical role in the activation of Ca2+-dependent apoptosis. In the cells overexpressing CRT, the intracellular calcium concentration was significantly increased and the activity of PKC and level of SECAR2a mRNA were reduced. Phosphorylation of Akt and ERKs decreased compared to control. In addition the activity of the anti-apoptotic factor, Bcl-2, was decreased and the activities of pro-apoptotic factor, Bax, p53 and caspase 8 were increased, leading to a dramatic augmentation of caspase 3 activity. Our results suggest that enhanced CRT expression in mature cardiomyocytes disrupts intracellular calcium regulation, leading to calcium-dependent apoptosis.
PLCδ1 protein rescues ischemia-reperfused heart by the regulation of calcium homeostasis.
Lim, Soyeon,Chang, Woochul,Cha, Min-Ji,Song, Byeong-Wook,Ham, Onju,Lee, Se-Yeon,Lee, Changyoun,Park, Jun-Hee,Lee, Sang-Kyou,Jang, Yangsoo,Hwang, Ki-Chul Academic Press 2014 MOLECULAR THERAPY Vol.22 No.6
<P>Myocardial Ca(2+) overload induced by ischemia/reperfusion (I/R) is a major element of myocardial dysfunction in heart failure. Phospholipase C (PLC) plays important roles in the regulation of the phosphoinositol pathway and Ca(2+) homeostasis in various types of cells. Here, we investigated the protective role of PLCδ1 against myocardial I/R injury through the regulation of Ca(2+) homeostasis. To investigate its role, PLCδ1 was fused to Hph1, a cell-permeable protein transduction domain (PTD), and treated into rat neonatal cardiomyocytes and rat hearts under respective hypoxia-reoxygenation (H/R) and ischemia-reperfusion conditions. Treatment with Hph1-PLCδ1 significantly inhibited intracellular Ca(2+) overload, reactive oxygen species generation, mitochondrial permeability transition pore opening, and mitochondrial membrane potential elevation in H/R neonatal cardiomyocytes, resulting in the inhibition of apoptosis. Intravenous injections of Hph1-PLCδ1 in rats with I/R-injured myocardium caused significant reductions in infarct size and apoptosis and also improved systolic and diastolic cardiac functioning. Furthermore, a small ions profile obtained using time-of-flight secondary ion mass spectrometry showed that treatment with Hph1-PLCδ1 leads to significant recovery of calcium-related ions toward normal levels in I/R-injured myocardium. These results suggest that Hph1-PLCδ1 may manifest as a promising cardioprotective drug due to its inhibition of the mitochondrial apoptotic pathway in cells suffering from I/R injury.</P>
Enhanced Calreticulin Expression Promotes Calcium-dependent Apoptosis in Postnatal Cardiomyocytes
Soyeon Lim,장우철,Byoung Kwon Lee,송희상,Ja Hyun Hong,Sunju Lee,송병욱,Hye-Jung Kim,Min-Ji Cha,장양수,정남식,최순용,황기철 한국분자세포생물학회 2008 Molecules and cells Vol.25 No.3
Calreticulin (CRT) is one of the major Ca2+ binding chaperone proteins of the endoplasmic reticulum (ER) and an unusual luminal ER protein. Postnatally elevated expression of CRT leads to impaired development of the cardiac conductive system and may be responsible for the pathology of complete heart block. In this study, the molecular mechanisms that affect Ca2+- dependent signal cascades were investigated using CRToverexpressing cardiomyocytes. In particular, we asked whether calreticulin plays a critical role in the activation of Ca2+-dependent apoptosis. In the cells overexpressing CRT, the intracellular calcium concentration was significantly increased and the activity of PKC and level of SECAR2a mRNA were reduced. Phosphorylation of Akt and ERKs decreased compared to control. In addition the activity of the anti-apoptotic factor, Bcl- 2, was decreased and the activities of pro-apoptotic factor, Bax, p53 and caspase 8 were increased, leading to a dramatic augmentation of caspase 3 activity. Our results suggest that enhanced CRT expression in mature cardiomyocytes disrupts intracellular calcium regulation, leading to calcium-dependent apoptosis.
전기화학적 수소발생반응을 위한 카본 페이퍼 위 NiCoS의 펄스 전기전착
임소연(Soyeon Lim),임태호(Taeho Lim) 한국세라믹학회 2022 세라미스트 Vol.25 No.2
NiCoS has good conductivity, and the sulfur it contains is known to improve the activity for hydrogen evolution reaction. Thus NiCoS has recently attracted much attention as a catalyst for hydrogen evolution reaction catalyst in neutral-pH water electrolysis. In this study, NiCoS was fabricated using pulse electrodeposition method and the effect of off time on the composition, morphology, and hydrogen evolution reaction activity was investigated. The physical and chemical characteristics of the catalyst were analyzed using field emission scanning electron microscopy, X-ray diffractometry, electrochemical impedance spectroscopy, etc. It was observed that the surface area of NiCoS, the sulfur content, and hydrogen evolution reaction activity of NiCoS increased together as the off time increased at a constant on time. The NiCoS with the highest sulfur content, produced by pulse electrodeposition, showed overpotentials of 262 and 285 mV to deliver current densities of 10, 50 mA/cm2, respectively, in the neutral pH region.
임유경(Yukyung Lim),김소연(Soyeon Kim),박윤우(Yoonwoo Park),김재희(Jaehee Kim),임지훈(Jihoon Lim),서연주(Yeonju Seo),임준규(Junkyu Lim),이태현(Taehyun Lee) 한국HCI학회 2023 한국HCI학회 학술대회 Vol.2023 No.2
코로나19로 인해 업무, 여가 생활 등의 주된 활동 장소가 주거 공간으로 바뀌었다. 특히 학교, 학원, 독서실, 카페와 같은 기존의 학습 공간 또한 주요 학습 환경이 주거 공간으로 변하며 타인의 시선을 통해 적절한 긴장 수준을 유지할 수 있는 이전과 달리 생활 공간과 분리되지 않아 생기는 집중 저해 요소 때문에 학생들은 어려움을 겪는다. 이러한 어려움을 극복하기 위해서 학생들은 다른 사람과 함께 있는 듯한 긴장 수준을 제공해주는 어플리케이션을을 활용하여 각자의 실시간 학습 상태를 공유하고 학습 몰입을 유지하려 노력한다. 본 연구에서는 이러한 배경을 바탕으로 포스트 코로나 시대의 새로운 디지털 경험 제공을 위해 머신 러닝을 활용한 실시간 상태 공유 비대면 학습 애플리케이션을 제안한다. 변화된 환경 속에서의 학습 경험을 이해하기 위해 12명의 학생을 대상으로 반구조화 심층 인터뷰와 에스노그래피를 실시하였다. 그 결과 학생들의 학습 몰입과 만족에 영향을 미치는 실시간 상태 공유 방식을 발견했고, 이를 바탕으로 주거 공간에서도 학습몰입을 경험할 수 있는 비대면 학습 애플리케이션을 제작하여 변화된 학습 환경에서의 학습 만족을 경험하도록 하였다.
Kim, Nayeong,Jeong, Soyeon,Jing, Kaipeng,Shin, Soyeon,Kim, Soyeon,Heo, Jun-Young,Kweon, Gi-Ryang,Park, Seung-Kiel,Wu, Tong,Park, Jong-Il,Lim, Kyu Hindawi Publishing Corporation 2015 BioMed research international Vol.2015 No.-
<P>The anticancer properties and mechanism of action of omega-3 polyunsaturated fatty acids (<I>ω</I>3-PUFAs) have been demonstrated in several cancers; however, the mechanism in lung cancer remains unclear. Here, we show that docosahexaenoic acid (DHA), a <I>ω</I>3-PUFA, induced apoptosis and autophagy in non-small cell lung cancer (NSCLC) cells. DHA-induced cell death was accompanied by AMP-activated protein kinase (AMPK) activation and inactivated phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling. Knocking down AMPK and overexpressing Akt increased mTOR activity and attenuated DHA-induced cell death, suggesting that DHA induces cell death via AMPK- and Akt-regulated mTOR inactivation. This was confirmed in Fat-1 transgenic mice, which produce <I>ω</I>3-PUFAs. Lewis lung cancer (LLC) tumor cells implanted into Fat-1 mice showed slower growth, lower phospho-Akt levels, and higher levels of apoptosis and autophagy than cells implanted into wild-type mice. Taken together, these data suggest that DHA-induced apoptosis and autophagy in NSCLC cells are associated with AMPK activation and PI3K/Akt inhibition, which in turn lead to suppression of mTOR; thus <I>ω</I>3-PUFAs may be utilized as potential therapeutic agents for NSCLC treatment.</P>