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- 저자 : 권아랑 (검색결과 4 건)
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SMURF1 Plays a Role in EGF-Induced Breast Cancer Cell Migration and Invasion
권아랑,백정화,이혜림,우경미,류현모 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.6
Epidermal growth factor (EGF) is a well-known growth factor that induces cancer cell migration and invasion. Previous studies have shown that SMAD ubiquitination regulatory factor 1 (SMURF1), an E3 ubiquitin ligase, regulates cell motility by inducing RhoA degradation. Therefore, we examined the role of SMURF1 in EGF-induced cell migration and invasion using MDA-MB-231 cells, a human breast cancer cell line. EGF increased SMURF1 expression at both the mRNA and protein levels. All ErbB family members were expressed in MDA-MB-231 cells and receptor tyrosine kinase inhibitors specific for the EGF receptor (EGFR) or ErbB2 blocked the EGF-mediated induction of SMURF1 expression. Within the signaling pathways examined, ERK1/2 and protein kinase C activity were required for EGF-induced SMURF1 expression. The overexpression of constitutively active MEK1 increased the SMURF1 to levels similar to those induced by EGF. SMURF1 induction by EGF treatment or by the overexpression of MEK1 or SMURF1 resulted in enhanced cell migration and inva-sion, whereas SMURF1 knockdown suppressed EGF- or MEK1-induced cell migration and invasion. EGF treatment or SMURF1 overexpression decreased the endogenous RhoA protein levels. The overexpression of constitutively active RhoA prevented EGF- or SMURF1-induced cell migration and invasion. These results suggest that EGF-induced SMURF1 plays a role in breast cancer cell migration and invasion through the downregulation of RhoA.
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Cut-Off Values for Visceral Fat Area Identifying Korean Adults at Risk for Metabolic Syndrome
이아랑,김예지,오승원,이철민,최호준,조희경,오범조,황승식,김승재,권오덕 대한가정의학회 2018 Korean Journal of Family Medicine Vol.39 No.4
Background: Cut-off values for visceral fat area (VFA) measured by computed tomography (CT) for identifying individualsat risk of metabolic syndrome (MetS) have not been clearly established in Korean adults, particularly forlarge populations. We aimed to identify optimal VFA and waist circumference (WC) cut-off values and compare theability of VFA and WC to predict the presence of ≥2 metabolic risk factors. Methods: We included 36,783 subjects aged 19–79 years undergoing abdominal fat CT during regular health checkupsbetween January 2007 and February 2015 in Seoul. The risk factors for MetS except WC were based on the InternationalDiabetes Federation criteria. Receiver operating characteristic curve analyses were used to determinethe appropriate VFA and WC cut-off values for MetS. Results: VFA was a more significant predictor of metabolic risk factors than WC and body mass index (BMI). Theoptimal cut-off values for VFA and WC were 134.6 cm2 and 88 cm for men and 91.1 cm2 and 81 cm for women, respectively. We estimated age-specific cut-off values for VFA, WC, and BMI. VFA cut-off values increased with age,particularly among women. Conclusion: This large population study proposed the cut-off values for VFA and WC for identifying subjects at riskof MetS among Korean adults. For more accurate diagnosis, different age-specific cut-off values for VFA and WCmay be considered.
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채화성,박현정,황효린,권아랑,임원희,이원진,한동헌,김영호,백정화 한국분자세포생물학회 2011 Molecules and cells Vol.32 No.2
Orthodontic force causes gradual compression of the periodontal ligament tissues, which leads to local hypoxia in the compression side of the tissues. In this study, we investigated whether antioxidants exert a regulatory effect on two factors: the expression of pro-inflammatory cytokines in human periodontal ligament fibroblasts (PDLFs)that were exposed to mechanical compression and hypoxia and the rate of orthodontic tooth movement in rats. Exposure of PDLFs to mechanical compression (0.5-3.0g/㎠) or hypoxic conditions increased the production of intracellular reactive oxygen species. Hypoxic treatment for 24 h increased the mRNA levels of IL-1β, IL-6 and IL-8as well as vascular endothelial growth factor (VEGF) in PDLFs. Resveratrol (10 nM) or N-acetylcysteine (NAC, 20mM) diminished the transcriptional activity of hypoxiainducible factor-1 and hypoxia-induced expression of VEGF. Combined treatment with mechanical compression and hypoxia significantly increased the expression levels of IL-1β, IL-6, IL-8, TNF-α and VEGF in PDLFs. These levels were suppressed by NAC and resveratrol. The maxillary first molars of rats were moved mesially for seven days using an orthodontic appliance. NAC decreased the amount of orthodontic tooth movement compared to the vehicletreated group. The results from immunohistochemical staining demonstrated that NAC suppressed the expression of IL-1β and TNF-α in the periodontal ligament tissues compared to the vehicle-treated group. These results suggest that antioxidants have the potential to negatively regulate the rate of orthodontic tooth movement through the down-regulation of pro-inflammatory cytokines in the compression sides of periodontal ligament tissues.
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Hyun-Jung Park,백정화,Kyung Hwa Baek,Hye-Lim Lee,권아랑,Hyo Rin Hwang,Abdul S. Qadir,우경미,류현모 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.6
During orthodontic tooth movement, local hypoxia and enhanced osteoclastogenesis are observed in the compression side of periodontal tissues. The receptor activator of nuclear factor-κB ligand (RANKL) is an osteoblast/stromal cell-derived factor that is essential for osteoclastogenesis. In this study, we examined the effect of hypoxia on RANKL expression in human periodontal ligament fibroblasts (PDLFs) to investigate the relationship between local hypoxia and enhanced osteoclastogenesis in the compression side of periodontal tissues. Hypoxia significantly enhanced the levels of RANKL mRNA and protein as well as hypoxia inducible factor-1α (HIF-1α) protein in PDLFs. Constitutively active HIF-1α alone significantly increased the levels of RANKL expression in PDLFs under normoxic conditions, whereas dominant negative HIF-1αblocked hypoxia-induced RANKL expression. To investigate further whether HIF-1α directly regulates RANKL transcription, a luciferase reporter assay was performed using the reporter vector containing the RANKL promoter sequence. Exposure to hypoxia or overexpression of constitutively active HIF-1α significantly increased RANKL promoter activity, whereas dominant negative HIF-1αblocked hypoxia-induced RANKL promoter activity. Furthermore,mutations of putative HIF-1α binding elements in RANKL promoter prevented hypoxia-induced RANKL promoter activity. The results of chromatin immunoprecipitation showed that hypoxia or constitutively active HIF-1α increased the DNA binding of HIF-1α to RANKL promoter. These results suggest that HIF-1α mediates hypoxia-induced up-regulation of RANKL expression and that in compression side periodontal ligament, hypoxia enhances osteoclastogenesis, at least in part, via an increased RANKL expression in PDLFs.
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