• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.4007-4011
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• 2012

Purpose: Retinoblastoma-interacting zinc finger gene (RIZ1) is a tumor suppressor gene which is highly inactivated by promoter hypermethylation in patients with liver fluke-related cholangiocarcinoma (CCA). Epigenetic aberration of this gene might withdraw the ability to restrain tumor cell proliferation and migration. We aimed to define the role of RIZ1 on cell proliferation and migration in CCA cell line. Materials and methods: Small interference RNA (siRNA) was used to knock down the expression of RIZ1 in a CCA-derived cell line in which cell proliferation and cell migration were performed. Results: A predominant nuclear localization of RIZ1 was observed. Reduction of RIZ1 by siRNA augmented cell proliferation and migration. Conclusion: The result suggested that RIZ1 might play a role in regulating cell proliferation and migration in CCA. Reduction of RIZ1 expression may aggravate the progression of CCA.

• 한국진공학회:학술대회논문집
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• 한국진공학회 2013년도 제44회 동계 정기학술대회 초록집
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• pp.526-526
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• 2013

Plasma technology isbeing developed for a range of medical applications including wound healing. However, the effect of plasma on many cells and tissues is unclear. Cell migration and cell proliferation are very important biological processes which are affected by plasma exposure and might be a potential target for plasma therapy during wound healing treatment. In this study, we confirmed the plasma exposure time and incubation time after plasma treatment in skin fibroblast (L-929 cells) to evaluate the optimal conditions forplasma exposure to the cell in-vitro. In addition, we used a scratch method to generate artificial wound for evaluating the cell migration by plasma treatment. Where, the cells were treated with plasma and migration rate was observed by live-cell imaging device. To find the cell proliferation, cell viability assay was executed. The results of this study indicate the increased cell proliferation and migration on mild plasma treatment. The mechanisms for cell migration and cell proliferation after plasma treatment for future studies will be discussed.

• Asian Pacific Journal of Cancer Prevention
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• 제15권15호
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• pp.6349-6352
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• 2014

The present study was undertaken to determine the roles of insulin in the growth of transplanted breast cancer in nude mice, and the proliferation and migration of MCF-7 human breast cancer cells and assess its influence on downstream signaling pathways. In a xenograft mouse model with injection of MCF-7 human breast cancer cells, tumor size was measured every other day. The insulin level and insulin receptor (IR) were increased in the breast cancer patient tissues. Insulin injected subcutaneously around the tumor site in mice caused increase in the size and weight of tumor masses, and promoted proliferation and migration of MCF-7 cells. The effects of insulin on the increase in the proliferation and migration of MCF-7 human breast cancer cells were abolished by pretreatment with the extracellular regulated kinase (ERK) inhibitor PD98059. Insulin increased the phosphorylation of ERK in the MCF-7 cells. These results indicate that insulin promotes the growth of breast cancer in nude mice, and increases the proliferation and migration of MCF-7 human breast cancer cells via the ERK pathway.

• 한국자원식물학회지
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• 제21권1호
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• pp.96-102
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• 2008

Nelumbo nucifera Gaertn.(family Nymphaeaceae) has been used for summer heat syndrome as home remedy in Japan, China and Korea. Although whole plant parts are edible, root is commonly consumed. It has been reported that rhizome extract showed anti-diabetic and anti-inflammatory effects. However, in spite of usefulness for treatment of various diseases, the effect of Nelumbo nucifera rhizome(NNR) on proliferation, migration and matrix degrading enzymes-matrix metalloproteinsases(MMPs), the expression of which degrades extracellular matrix(ECM) leading to metastasis, has not been fully elucidated. We examined the effect of hot water extract of NNR on the proliferation, migration and secretion of MMP-2 and MMP-9 in rat smooth muscle cells(rSMC), epidermoid cancer cells(A431) and breast cancer cells(MDA-MB-231). The proliferation assay was carried out using MTT assay, the principle of which depends upon the conversion of MTT by mitochondrial dehydrogensases of viable cells to formazan crystals. The effect of NNR on migration of cells was examined using wound healing assay. Our results showed that there was inhibition in the proliferation, migration and expression of MMP-2 and MMP-9 in dose dependent fashion in all the cells used. Thus, we concluded that NNR could be used as traditional medicine in the treatment of various diseases where proliferation, migration and MMPs' expression plays a pathological role like in restenosis and metastasis.

• 한국임상수의학회지
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• 제36권4호
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• pp.200-206
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• 2019

This study was performed to assess the anti-inflammatory and cartilage regenerative effects of platelet-rich plasma (PRP) on canine chondrocytes. Proliferation and migration assays under both normal and lipopolysaccharide (LPS)-induced inflammatory conditions were performed with various concentrations of PRP (1% to 10%). The expression levels of genes related to osteoarthritis were evaluated in the following groups: PRP group, LPS group and LPS + PRP group. mRNA expression levels were detected using real-time polymerase chain reaction (RT-PCR). Proliferation assays showed significantly enhanced proliferation in all PRP-treated groups compared with the no serum group. Compared with 10% fetal bovine serum (FBS), PRP concentrations above 3% in the normal condition and 1% to 7% PRP in the LPS-induced inflammatory condition were found to significantly promote chondrocyte proliferation. In the normal condition, all PRP-treated groups showed significantly increased cell migration compared with the no serum group. Chondrocyte migration was decreased with LPS-induced inflammation, but PRP treatment resulted in significantly enhanced migration compared with the other groups in this condition. According to RT-PCR, the LPS + PRP group showed significantly higher levels of COL1A1, IL-6, aggrecan and lower levels of $TNF-{\alpha}$, MMP-1, MMP-3 mRNA expression compared to the LPS group. The results of this study suggest that PRP application can enhance the proliferation and migration of canine chondrocytes and improve canine articular cartilage regeneration.

• BMB Reports
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• 제55권5호
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• pp.244-249
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• 2022

Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway.

• 한국임상수의학회지
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• 제37권4호
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• pp.198-203
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• 2020

Synovial fluid (SF) contains various factors which may be helpful for corneal stromal healing, such as cytokines, growth factors, hyaluronic acid, and proteins. Therefore, the purpose of this study was to determine the effect of SF on proliferation and migration in canine keratocytes. In order to evaluate the degree of proliferation and migration, canine keratocytes were cultured in DMEM containing 1%, 3%, 5%, or 10% SF. Real-time PCR was performed in a control group and the group treated with 5% SF, in order to measure the expression levels of factors associated with corneal wound healing. These factors included interleukin-1α (IL-1α), hepatocyte growth factor (HGF), transforming growth factor-β (TGF-β), and α-smooth muscle actin (SMA-α). Proliferation assays demonstrated that proliferation was significantly enhanced in groups treated with greater than 3% SF, as compared with that of the control group. In addition, migration in all SF-treated groups was significantly increased as compared with migration in the control group, as measured by migration assays. mRNA expression of IL-1α and HGF was significantly increased and mRNA expression of TGF-β and SMA-α was significantly decreased in the cells treated with 5% SF. These findings suggest that SF may promote corneal wound healing.

• Journal of Microbiology and Biotechnology
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• 제32권6호
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• pp.792-799
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• 2022

As a vital problem in reproductive health, recurrent spontaneous abortion (RSA) affects about 1% of women. We performed this study with an aim to explore the molecular mechanism of interleukin-23 (IL-23) and find optimal or effective methods to improve RSA. First, ELISA was applied to evaluate the expressions of IL-23 and its receptor in HTR-8/SVneo cells after IL-23 treatment. CCK-8, TUNEL, wound healing and transwell assays were employed to assess the proliferation, apoptosis, migration and invasion of HTR-8/SVneo cells, respectively. Additionally, the expressions of apoptosis-, migration-, epithelial-mesenchymal transition- (EMT-) and p38 MAPK signaling pathway-related proteins were measured by western blotting. To further investigate the relationship between IL-23 and p38 MAPK signaling pathway, HTR-8/SVneo cells were treated for 1 h with p38 MAPK inhibitor SB239063, followed by a series of cellular experiments on proliferation, apoptosis, migration and invasion, as aforementioned. The results showed that IL-23 and its receptors were greatly elevated in IL-23-treated HTR-8/SVneo cells. Additionally, IL-23 demonstrated suppressive effects on the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells. More importantly, the molecular mechanism of IL-23 was revealed in this study; that is to say, IL-23 inhibited the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells via activating p38 MAPK signaling pathway. In conclusion, IL-23 inhibits trophoblast proliferation, migration, and EMT via activating p38 MAPK signaling pathway, suggesting that IL-23 might be a novel target for the improvement of RSA.

• The Korean Journal of Physiology and Pharmacology
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• 제19권6호
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• pp.499-506
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• 2015

Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.

• Biomolecules & Therapeutics
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• 제25권4호
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• pp.354-361
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• 2017

Transcriptional co-activator with a PDZ-binding motif (TAZ) is an important factor in lysophosphatidic acid (LPA)-induced promotion of migration and proliferation of human mesenchymal stem cells (MSCs). The expression of TAZ significantly increased at 6 h after LPA treatment, and TAZ knockdown inhibited the LPA-induced migration and proliferation of MSCs. In addition, embryonic fibroblasts from TAZ knockout mice exhibited the reduction in LPA-induced migration and proliferation. The LPA1 receptor inhibitor Ki16425 blocked LPA responses in MSCs. Although TAZ knockdown or knockout did not reduce LPA-induced phosphorylation of ERK and AKT, the MEK inhibitor U0126 or the ROCK inhibitor Y27632 blocked LPA-induced TAZ expression along with the reduction in the proliferation and migration of MSCs. Our data suggest that TAZ is an important mediator of LPA signaling in MSCs in the downstream of MEK and ROCK signaling.