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Therapeutic effects of ginsenosides on breast cancer growth and metastasis
Yujin Jin,Diem Thi Ngoc Huynh,Thuy Le Lam Nguyen,Hyesu Jeon,Kyung-Sun Heo 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.8
Breast cancer is the most common cause ofcancer-related deaths among women worldwide. Thus, thedevelopment of new and eff ective low-toxicity drugs is vital. The specifi c characteristics of breast cancer have allowed forthe development of targeted therapy towards each breast cancersubtype. Nevertheless, increasing drug resistance is displayedby the changing phenotype and microenvironmentsof the tumor through mutation or dysregulation of variousmechanisms. Recently, emerging data on the therapeuticpotential of biocompounds isolated from ginseng have beenreported. Therefore, in this review, various roles of ginsenosidesin the treatment of breast cancer, including apoptosis,autophagy, metastasis, epithelial-mesenchymal transition,epigenetic changes, combination therapy, and drug deliverysystem, have been discussed.
Yujin Jin,Hyesu Jeon,Thuy Le Lam Nguyen,Lila Kim,Kyung-Sun Heo 대한약학회 2023 Archives of Pharmacal Research Vol.46 No.12
Acute lung injury (ALI) is the leading cause of respiratory diseases induced by uncontrolled inflammation and cell death. Lipopolysaccharide (LPS) is a major trigger of ALI in the progression through macrophage differentiation and the accelerated release of pro-inflammatory cytokines. The present study aimed to investigate the protective effects of human milk oligosaccharides, specifically 3′-sialyllactose (3′-SL) and 6′-sialyllactose (6′-SL), on LPS-induced ALI and elucidate their underlying signaling pathways. The inhibitory effects of 3′-SL and 6′-SL on inflammation were evaluated using LPS-treated RAW 264.7 macrophages. To establish the ALI model, mice were treated with 10 mg/kg LPS for 24 h. Histological changes in the lung tissues were assessed using hematoxylin and eosin staining and immunofluorescence. LPS causes thickening of the alveolar wall infiltration of immune cells in lung tissues and increased serum levels of TNF-α, IL-1β, and GM-CSF. However, these effects were significantly alleviated by 100 mg/kg of 3′-SL and 6′-SL. Consistent with the inhibitory effects of 3′-SL and 6′-SL on LPS-induced pro-inflammatory cytokine secretion in serum, 3′-SL and 6′-SL suppressed mRNA expression of TNF-α, IL-1β, MCP-1, iNOS, and COX2 in LPS-induced RAW 264.7 cells. Mechanistically, 3′-SL and 6′-SL abolished LPS-mediated phosphorylation of NF-κB and STAT1. Interestingly, fludarabine treatment, a STAT1 inhibitor, did not affect LPS-mediated NF-κB phosphorylation. In summary, 3′-SL and 6′-SL protect LPS-induced macrophage activation and ALI through the STAT1 and NF-κB signaling pathways.
( Yujin Jin ),( Diem Thi Ngoc Huynh ),( Keon Wook Kang ),( Chang-seon Myung ),( Kyung-sun Heo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.12
Cisplatin (Cis-DDP) is one of the most widely used anti-cancer drugs. It is applicable to many types of cancer, including lung, bladder, and breast cancer. However, its use is now limited because of drug resistance. p90 ribosomal S6 kinase (p90RSK) is one of the downstream effectors in the extracellular signalregulated protein kinases 1 and 2 (ERK1/2) pathway and high expression of p90RSK is observed in human breast cancer tissues. Therefore, we investigated the role of p90RSK in the Cis-DDP resistance-related signaling pathway and epithelial-mesenchymal transition (EMT) in breast cancer cells. First, we discovered that MDA-MB-231 cells exhibited more Cis-DDP resistance than other breast cancer cells, including MCF-7 and BT549 cells. Cis-DDP increased p90RSK activation, whereas the inactivation of p90RSK using a small interfering RNA (siRNA) or dominant-negative kinase mutant plasmid overexpression significantly reduced Cis-DDP-induced cell proliferation and migration via the inhibition of matrix metallopeptidase (MMP)2 and MMP9 in MDA-MB-231 cells. In addition, p90RSK activation was involved in EMT via the upregulation of mRNA expression, including that of Snail, Twist, ZEB1, N-cadherin, and vimentin. We also investigated NF-κB, the upstream regulator of EMT markers, and discovered that Cis-DDP treatment led to NF-κB translocation in the nucleus as well as its promoter activity. Our results suggest that targeting p90RSK would be a good strategy to increase Cis-DDP sensitivity in triple-negative breast cancers. [BMB Reports 2019; 52(12): 706-711]
Virus-Based Structural Color Sensor for the Endocrine Disrupting Chemicals Detection
Yujin Lee,Ye-Ji Kim,Thanh Mien Nguyen,Yeong Ju Lee,You Hwan Kim,Seung Su Jeong,Jae Suk Yoon,Na Yeung Kim,Jun Su Choi,Min Soo Kim,Jin Jae Park,Suk Ho Lee,Eun Jung Choi,Jin-Woo Oh 한국고분자학회 2019 한국고분자학회 학술대회 연구논문 초록집 Vol.44 No.2
Yujin Jin,허경선 대한미생물학회 2019 Journal of Bacteriology and Virology Vol.49 No.4
p90 ribosomal S6 kinase (p90RSK), one of the downstream effectors in ERK1/2 pathways, shows high expression in human breast cancer tissues. However, its role in breast cancer development and drug resistance is not fully understood. Here, we demonstrate that Cis-DDP treatment failed to increase cytotoxicity in MDA-MB-231 cells compared to MCF-7 cells and p90RSK activation was involved in Cis-DDP-resistance to MDA-MB-231 cells. In the study, we found that inhibition of p90RSK expression or activation using a small interfering RNA (siRNA) or dominant-negative kinase mutant (DN-p90RSK) plasmid overexpression increased Cis-DDP-induced cytotoxicity of MDA-MB-231 cells, respectively. Mechanistically, we found that Cis-DDP resistance was associated with up-regulation of epithelial growth factor (EGF) expression and EGF treatment induced cancer survival signaling pathway including activation of ERK1/2, p90RSK, and Akt. We also examined the expression of epithelial-mesenchymal transition (EMT)-associated proteins using a reverse transition-quantitative PCR analysis. Cis-DDP treatment induced EMT by increasing the expression levels of N-cadherin, Snail, and Twist, while decreasing the expression levels of E-cadherin. Furthermore, we examined the epithelial marker, Zonula occludens-1 (ZO-1) using immunofluorescence analysis and found that Cis-DDP-inhibited ZO-1 expression was recovered by p90RSK deactivated condition. Therefore, we conclude that Cis-DDP resistance is involved in EMT via regulating the EGF-mediated p90RSK signaling pathway in MDA-MB-231 cells.
Yujin Jin,Diem Thi Ngoc Huynh,Kyung-Sun Heo 대한약학회 2022 Archives of Pharmacal Research Vol.45 No.3
Ginsenoside-Rh1 (Rh1) is a ginseng-derivedcompound that has been reported to exert anticancer eff ectsby regulating cell cycle arrest and apoptosis according toreactive oxygen species (ROS) production. However, theeff ects of Rh1 on mitochondrial dysfunction are involved intriple negative breast cancer (TNBC) cell apoptosis, and therelated molecular mechanisms remain unknown. Rh1 treatmentinduced cell toxicity less than 50% at 50 μM. In addition,Rh1 induced apoptosis in TNBC cells through cleavedcaspase-3 activation and G1/S arrest. The Rh1-treatedTNBC cells showed a signifi cant increase in mitochondrialROS (mtROS), which in turn increased protein expressionof mitochondrial molecules, such as Bak and cytochromeC, and caused the loss of mitochondrial membrane potential. Pretreatment with mitochondria-targeted antioxidantMito-TEMPO alters the Rh1-reduced rate of mito- andglycol-ATP. Furthermore, Rh1 induces ER stress-mediatedcalcium accumulation via PERK/eIF2α/ATF4/CHOP pathway. Inhibition of ATF4 by siRNA transfection signifi cantlyinhibited Rh1-mediated apoptosis and calcium production. Interestingly, Mito-TEMPO treatment signifi cantly reducedapoptosis and ER stress induced by Rh1. Finally, Rh1 at5 mg/kg suppressed tumor growth through increased levelsof ROS production, cleaved caspase-3, and ATF4 more than5-fl uorouracil treated group. Overall, our results suggest thatRh1 has potential for use in TNBC treatment.
Jin, Yujin,Yang, Sungwhan,Im, Sungoh,Jeong, Won-Joong,Park, EunJeong,Choi, Dong-Woog The Korean Society of Plant Biotechnology 2017 식물생명공학회지 Vol.44 No.3
Water temperature is one of the major factors that impacts the growth and life cycle of Pyropia tenera, one of the most valuable and cultivated marine red algae belonging to Bangiales (Rhodophytes). We analyzed transcriptome from gametophyte of P. tenera under normal and high temperature conditions, and identified four small heat shock proteins (sHSPs). They have no significant amino acid sequence homology with known proteins in public databases except PhsHSP22 from Pyropia haitanensis. PtsHSP19.3 gene responded to high temperature but slightly or not to desiccation, freezing or high salt condition. When the PtsHSP19.3 gene was overexpressed in Chlamydomonas reinhardtii, transformed Chlamydomonas lines revealed much higher growth rate than that of control cells under heat stress condition. Transformed cells also grew well in those of the control cell onto the medium containing high salt or $H_2O_2$. When the PtsHSP19.3 was fused to GFP and introduced into tobacco protoplast, fluorescence was detected at several spots. Results indicate that PtsHSP19.3 may form super-molecular assembles and be involved in tolerance to heat stress.