• Journal of Applied Biological Chemistry
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• v.57 no.2
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• pp.103-111
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• 2014

A1E is an extract from traditional Asian medicinal plants that has therapeutic activities against cancers, metabolic disease, and other intractable conditions. However, its mechanism of action on cervical cancer has not been studied. In order to ascertain if A1E would have pronounced anti-cervical cancer effect, cervical cancer cells were incubated with A1E and apoptosis was detected by nuclear morphological changes, annexin V-FITC/PI staining, cell cycle analysis, western blotting, Reverse-transcription polymerase chain reaction, and measurement of mitochondrial membrane potential. Expression of human papiloma virus E6 and E7 oncogenes was down-regulated in A1E-treated cervical cancer cells, while p53 and retinoblastoma protein levels were enhanced. A1E also perturbed cell cycle progression at sub-G1 and altered cell cycle regulatory factors in SiHa cervical cancer cells. A1E activated apoptotic intrinsic pathway markers such as caspase-9, caspase-3 and poly ADP-ribose polymerase, and down-regulated expression of Bcl-2 and Bcl-xl. A1E induced mitochondrial membrane potential collapse and cytochrome c release, and inhibited phosphatidylinositol 3-kinase (PI3K)/Akt, key factors involved in cell survival signaling. Taken all these results, A1E induced apoptosis via activation of the intrinsic pathway and inhibition of the PI3K/Akt survival-signaling pathway in SiHa cervical cancer cells. In conclusion, A1E exerts anti-proliferative action growth inhibition on cervical cancer cells through apoptosis which demonstrates its anti-cervical cancer properties.

• Journal of Life Science
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• v.32 no.1
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• pp.63-69
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• 2022

The thioredoxin reductase (TrxR) system is essential for cell survival and function by playing a pivotal role in maintaining homeostasis of cellular redox and regulating signal transduction pathways. The TrxR system comprises thioredoxin (Trx), TrxR, and nicotinamide adenine dinucleotide phosphate. Trx reduced by the catalytic reaction of the TrxR enzyme reduces downstream proteins, resulting in protection against oxidative stress and regulation of cell differentiation, growth, and death. Cancer cells survive by improving their intracellular antioxidant capacity to eliminate excessively generated reactive oxygen species (ROS) due to infinite cell proliferation and a high metabolic rate. Therefore, cancer cells have high dependence and sensitivity to antioxidant systems, suggesting that focusing on TrxR, a representative antioxidant system, is a potential strategy for cancer therapy. Several studies have revealed that TrxR is expressed at high levels in various types of cancers, and research on anticancer activity targeting the TrxR system is increasing. In this review, we discuss the feasibility and value of the TrxR system as a strategy for anticancer activity research by examining the relationship between the function of the intracellular TrxR system and the development and progression of cancer, considering the anticancer activity and mechanism of TrxR inhibitors.

• Journal of Life Science
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• v.33 no.8
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• pp.651-662
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• 2023

Peroxisomes, known as microbodies, are a class of morphologically similar subcellular organelles commonly found in most eukaryotic cells. They are 0.2~1.8 ㎛ in diameter and are bound by a single membrane. The matrix is usually finely granular, but occasionally crystalline or fibrillary inclusions are observed. They characteristically contain hydrogen peroxide (H₂O₂) generating oxidases and contain the enzyme catalase, thus confining the metabolism of the poisonous H₂O₂ within these organelles. Therefore, the eukaryotic organelles are greatly dynamic both in morphology and metabolism. Plant peroxisomes, in particular, are associated with numerous metabolic processes, including β-oxidation, the glyoxylate cycle and photorespiration. Furthermore, plant peroxisomes are involved in development, along with responses to stresses such as the synthesis of important phytohormones of auxins, salicylic acid and jasmonic acids. In the past few decades substantial progress has been made in the study of peroxisome biogenesis in eukaryotic organisms, mainly in animals and yeasts. Advancement of sophisticated techniques in molecular biology and widening of the range of genomic applications have led to the identification of most peroxisomal genes and proteins (peroxins, PEXs). Furthermore, recent applications of proteome study have produced fundamental information on biogenesis in plant peroxisomes, together with improving our understanding of peroxisomal protein targeting, regulation, and degradation. Nonetheless, despite this progress in peroxisome development, much remains to be explained about how peroxisomes originate from the endoplasmic reticulum (ER), then assemble and divide. Peroxisomes perform dynamic roles in many phases of plant development, and in this review, we focus on the latest progress in furthering our understanding of plant peroxisome functions, biogenesis, and dynamics.

• 한국체육학회지인문사회과학편
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• v.55 no.2
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• pp.603-615
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• 2016

This study was conducted by performing intensities aerobic exercise for 12 weeks, three times a week targeting 28 middle aged women. The purpose of this study was analyzing factors which affect cognitive function and changes of blood pressure, renin-aldosterone system, neurotransmitter, cognitive function and working memory after treatment. The participants were divided into three groups which are the control group(n=9, non exercise), moderate intensity aerobic exercise group(n=10, 50%V02max), high intensity aerobic exercise group(n=9, 70%V02max). The two-way ANOVA(repeated measure) and multiple regression analysis were carried out to target those three groups before and after treatment. The results were as follows like this. The moderate intensity aerobic exercise increased renin, brain derived neurotrophic factor(BDNF), cognitive function and working memory. Also, it reduced aldosterone, angiotensinII and aldosterone-renin ratio. The high intensity aerobic exercise showed increase BDNF, cognitive function and working memory and decrease systolic. As a result of a multiple regression analysis of factors affecting cognitive function after intensities aerobic exercise, the moderate intensity aerobic exercise affected diastolic blood pressure, decrease of aldosterone-renin ratio and working memory. Also, an increase of BDNF affected cognitive function, the high intensity aerobic exercise affected working memory BDNF and an increase of serotonin affected cognitive function. Therefore, It could be seen that more than moderate intensity exercise increase woman's cognitive function and working memory. Also, there were metabolic factors which affect the increase of cognitive function. To moderate intensity exercise, renin-aldosterone and working memory affected to increase of cognitive function. For high intensity exercise, BDNF and working memory affected to it.

• Nutrition Research and Practice
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• v.18 no.1
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• pp.1-18
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• 2024

BACKGROUND/OBJECTIVES: Endoplasmic reticulum (ER) stress in adipose tissue causes an inflammatory response and leads to metabolic diseases. However, the association between vitamin D and adipose ER stress remains poorly understood. In this study, we investigated whether 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) alleviates ER stress in adipocytes. MATERIALS/METHODS: 3T3-L1 cells were treated with different concentrations (i.e., 10-100 nM) of 1,25(OH)₂D₃ after or during differentiation (i.e., on day 0-7, 3-7, or 7). They were then incubated with thapsigargin (TG, 500 nM) for an additional 24 h to induce ER stress. Next, we measured the mRNA and protein levels of genes involved in unfold protein response (UPR) and adipogenesis using real-time polymerase chain reaction and western blotting and quantified the secreted protein levels of pro-inflammatory cytokines. Finally, the mRNA levels of UPR pathway genes were measured in adipocytes transfected with siRNA-targeting Vdr. RESULTS: Treatment with 1,25(OH)₂D₃ during various stages of adipocyte differentiation significantly inhibited ER stress induced by TG. In fully differentiated 3T3-L1 adipocytes, 1,25(OH)₂D₃ treatment suppressed mRNA levels of Ddit3, sXbp1, and Atf4 and decreased the secretion of monocyte chemoattractant protein-1, interleukin-6, and tumor necrosis factor-α. However, downregulation of the mRNA levels of Ddit3, sXbp1, and Atf4 following 1,25(OH)₂D₃ administration was not observed in Vdr-knockdown adipocytes. In addition, exposure of 3T3-L1 preadipocytes to 1,25(OH)₂D₃ inhibited transcription of Ddit3, sXbp1, Atf4, Bip, and Atf6 and reduced the p-alpha subunit of translation initiation factor 2 (eIF2α)/eIF2α and p-protein kinase RNA-like ER kinase (PERK)/PERK protein ratios. Furthermore, 1,25(OH)₂D₃ treatment before adipocyte differentiation reduced adipogenesis and the mRNA levels of adipogenic genes. CONCLUSIONS: Our data suggest that 1,25(OH)₂D₃ prevents TG-induced ER stress and inflammatory responses in mature adipocytes by downregulating UPR signaling via binding with Vdr. In addition, the inhibition of adipogenesis by vitamin D may contribute to the reduction of ER stress in adipocytes.