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        Quercetin-3-O-glucoside suppresses pancreatic cancer cell migration induced by tumor-deteriorated growth factors in vitro

        LEE, JUNGWHOI,LEE, JUNGSUL,KIM, SEUNG JUN,KIM, JAE HOON Spandidos Publications 2016 ONCOLOGY REPORTS Vol.35 No.4

        <P>Analysis using Universal exPress Codes (UPCs) with the public microarray database GEO indicates significantly higher mRNA expressions of VEGF-A, bFGF, and bFGFR2 in pancreatic cancers than those in normal pancreatic tissues. Human pancreatic cancer cell line CFPAC-1 and SNU-213 had relatively differential sensitivity to exogenous VEGF-A, bFGF, and TGF-beta 1 in migration property. Treatment of quercetin-3-O-glucoside suppressed the migratory activity induced by TGF-(3 and VEGF-A even at relatively low dosages in CFPAC-1, but not in bFGF-activated SNU-213 cells. However, high dosages of quercetin-3-O-glucoside sufficiently suppressed the migratory activity induced by bFGF in SNU-213 cells. Furthermore, co-treatment with low dose of gemcitabine plus quercetin-3-O-glucoside showed synergistic inhibition effects on the infiltrate activity induced by bFGF in CFPAC-1 and SNU-213 cells. These results collectively suggested that quercetin-3-O glucoside could act as an inhibitor of local metastasis induced by various growth factors in pancreatic cancers and be an effective adjuvant to boost chemotherapeutic efficacy of gemcitabine, currently used in pancreatic cancers.</P>

      • KCI등재

        VSTM2L is a promising therapeutic target and a prognostic soluble-biomarker in cholangiocarcinoma

        Jungwhoi Lee,Woogwang Sim,Jungsul Lee,Jae-Hoon Kim 생화학분자생물학회 2024 BMB Reports Vol.57 No.7

        The aim of the present study is to provide a rational backgroundfor silencing the V-set and transmembrane domain containing2 like (VSTM2L) in consort with recognising solubleVSTM2L against cholangiocarcinoma. A therapeutic target againstcholangiocarcinoma was selected using iterative patient partitioning(IPP) calculation, and it was verified by in vitro and insilico analyses. VSTM2L was selected as a potential therapeutictarget against cholangiocarcinoma. Silencing the VSTM2L expressionsignificantly attenuated the viability and survival ofcholangiocarcinoma cells through blockade of the intracellularsignalling pathway. In silico analysis showed that VSTM2L affectedthe positive regulation of cell growth in cholangiocarcinoma. Liptak’s z value revealed that the expression of VSTM2Lworsened the prognosis of cholangiocarcinoma patients. In addition,soluble VSTM2L was significantly detected in the wholeblood of cholangiocarcinoma patients compared with that ofhealthy donors. Our report reveals that VSTM2L might be thepotential therapeutic target and a soluble prognostic biomarkeragainst cholangiocarcinoma.

      • Anti-inflammatory effects of red beet extract by steaming time

        Song-I Han,Jungwhoi Lee,Jae-Hoon Kim 한국식품영양과학회 2021 한국식품영양과학회 학술대회발표집 Vol.2021 No.10

        The present study aimed to investigate the anti-inflammatory effects of red beet extract by differing the steaming time. The pH decreased from 6.2 to 4.0 by number of steaming treatment. On the other hand, contents of reducing sugar was increased on processing methods. As the times of steaming processes increased, DPPH radical scavenging activities and total phenol contents increased. We investigated the effect of steamed red beet extract on nitric oxide (NO) production in LPS-induced RAW264.7 cells. The 4 and 5 times steaming processes of red beet extract showed a higher NO production inhibitory effect at 200 μg/mL concentration. In addition, the red beet extract reduced interleukin- 6 (IL-6) production by steaming processes. These results suggest that steamed red beet extract can be a potential source as a anti-inflammatory agent.

      • KCI등재

        석결명이 TGF-β1로 유도된 망막색소상피세포의 증식에 미치는 영향

        한송이(Song-I Han),이중회(Jungwhoi Lee),김재훈(Jae-Hoon Kim) 한국산학기술학회 2023 한국산학기술학회논문지 Vol.24 No.8

        본 연구는 석결명을 초산화 하여 추출물을 획득하고, 초산화한 석결명 추출물이 TGF-β1로 유도된 망막색소상피세포에서의 전이에 미치는 영향과 그 기본 메커니즘을 조사하고자 하였다. 먼저 석결명 가루를 초산화 과정을 거쳐 추출한 후 초산화한 석결명 추출물의 세포 독성을 확인하고자 WST-1 assay법을 이용하여 측정하였고, TGF-β1과 초산화한 석결명 추출물을 동시에 망막색소상피세포에 처리한 후 morphology의 변화를 확인한 결과 TGF-β1으로 신장된 망막색소상피세포의 증식을 약 40%로 감소시켰다. 또한 이동능을 확인하기 위해 wound healing assay를 한 결과 초산화한 석결명 추출물이 망막색소상피세포에서 TGF-β1에 의한 이동능을 약 20% 억제하는 것을 확인하였다. 다음으로 초산화한 석결명 추출물을 처리한 망막색소상피세포에서 기본 메커니즘을 확인하기 위해 western blot을 수행하였다. MMP-2와 인산화된 FAK의 단백질 발현 수준을 확인한 결과 초산화한 석결명 추출물에 의해 감소하는 것을 확인하였다. 이러한 결과는 초산화된 석결명 추출물이 TGF-β1에 의해 유도된 망막색소상피세포의 증식과 전이를 억제하며 TGF-β1에 의해 촉진되어 병인으로 작용하는 증식유리체망막병증과 같은 망막질환을 예방하는데 도움이 될 것으로 기대된다. In this study, an extract was obtained by super-oxidizing abalone shell. The effect of super-oxidized abalone shell extract (SA) on TGF-β1-induced retinal pigment epithelial cell metastasis and its fundamental mechanism was investigated. First, abalone shell powder was extracted through a superoxidation process and measured using the WST-1 assay method to confirm the cytotoxicity. After treating retinal pigment epithelial cells with TGF-β1 and SA, the change in morphology was confirmed. TGF-β1 reduced the proliferation of elongated retinal pigment epithelial cells by approximately 40%. In addition, the wound healing assay to confirm the migratory ability confirmed that SA inhibited the migratory ability by TGF-β1 by approximately 20% in retinal pigment epithelial cells. Western blot was performed to confirm the basic mechanism in retinal pigment epithelial cells treated with SA. The protein expression levels of MMP-2 and phosphorylated FAK confirmed that they were decreased by SA. These results are expected to inhibit the proliferation and metastasis of retinal pigment epithelial cells induced by TGF-β1 and help prevent retinal diseases, such as proliferative vitreoretinopathy promoted by TGF-β1.

      • SCOPUSKCI등재

        Juniperus chinensis extract induces apoptosis via reaction oxygen species (ROS) generation in human pancreatic cancer cell lines

        ( Boram Go ),( Song-i Han ),( Jungwhoi Lee ),( Da-hye Kim ),( Chang-sook Kim ),( Jae Hoon Kim ) 한국응용생명화학회 2020 Journal of Applied Biological Chemistry (J. Appl. Vol.63 No.4

        Pancreatic cancer is among the most difficult-to-treat tumors. More than half of patients with this cancer have very few symptoms at the early stages, allowing the development of distant metastases and resistance to cancer treatment. In this study, we found that Juniperus chinensis extract (JCX) decreased the cell viability and migration activity of PANC-1 and SNU-213 pancreatic cancer cells in a dose-dependent manner. JCX increased caspase- 3 activation and generation of reactive oxygen species (ROS). Nacetylcysteine treatment blocked JCX-induced ROS generation and the negative effects on pancreatic cancer cell viability. In addition, JCX down-regulated the levels of phospho-focal adhesion kinase (p-FAK) and phospho-extracellular signal-regulated kinase (p-ERK). Together, these results indicate that JCX induces apoptosis in human pancreatic cancer cell lines through ROS production, downregulating FAK/ERK signaling and activating caspase-3. We propose that JCX-derived compounds represent candidates for the development of alternative medicines for the treatment of pancreatic cancer.

      • KCI등재

        Eriodictyol induces apoptosis via regulating phosphorylation of JNK, ERK, and FAK/AKT in pancreatic cancer cells

        Ui Hyeon Oh,Kim Da-Hye,Lee Jungwhoi,Han Song-I,Kim Jae-Hoon 한국응용생명화학회 2022 Journal of Applied Biological Chemistry (J. Appl. Vol.65 No.2

        Although it has been intensively studied over the past few decades, pancreatic cancer remains one of the most lethal cancers. Eriodictyol, a plant-derived flavonoid mainly found in citrus fruits, exerts diverse biological effects, including antioxidant, anti-cancer, and anti-inflammatory properties. In this study, we investigated the anticancer properties of eriodictyol and its mechanisms of action in pancreatic cancer cells. In both SNU213 and Panc-1 cells, eriodictyol decreased viability, induced apoptosis, and decreased clonogenicity. In addition, eriodictyol treatment increased the phosphorylation level of JNK and decreased the phosphorylation levels of ERK, FAK, and AKT. These observations provide insight into the molecular mechanisms of eriodictyol-induced apoptosis in pancreatic cancer cell lines, and could contribute to the development of candidate compounds for treating pancreatic cancer.

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