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Membrane cholesterol is required for activity of Vibrio vulnificus cytolysin
Yu, Hong-Nu,Lee, Young-Rae,Park, Kwang-Hyun,Rah, So-Young,Noh, Eun-Mi,Song, Eun-Kyung,Han, Myung-Kwan,Kim, Byeong-Soo,Lee, Sung-Ho,Kim, Jong-Suk 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10
Vibrio vulnificus cytolysin (VVC) forms a pore in the plasma membrane and induces cytolysis of various cells including erythrocytes, neutrophil and endothelial cells. The cytolytic activity of VVC is inhibited by exogenously added cholesterol, suggesting that membrane cholesterol might be required for VVC cytolytic activity. However, there is no direct evidence that membrane cholesterol is involved in VVC-induced cytolysis. Herein we demonstrate that membrane cholesterol is required for binding of VVC to the plasma membrane. Membrane cholesterol depletion with methyl-β-cyclodextrin inhibited VVC-induced K^(+) release, 2-deoxy glucose release and Ca^(2+) influx, which are indicators of VVC pore formation. The cholesterol depletion-induced blockage of VVC cytolysis was due to the inhibition of VVC binding to membrane. These findings suggest that interaction with cholesterol is required for activity of VVC.
On-Yu Hong,Sang Yull Kang,Eun-Mi Noh,Hong-Nu Yu,Hye-Yeon Jang,Seong-Hun Kim,Jingyu Hong,Eun Yong Chung,Jong-Suk Kim 생화학분자생물학회 2022 BMB Reports Vol.55 No.2
Aurora kinase is a family of serine/threonine kinases intimatelyassociated with mitotic progression and the development ofhuman cancers. Studies have shown that aurora kinases areimportant for the protein kinase C (PKC)-induced invasion ofcolon cancer cells. Recent studies have shown that aurora kinaseA promotes distant metastasis by inducing epithelial-to-mesenchymaltransition (EMT) in colon cancer cells. However, the roleof aurora kinase A in colon cancer metastasis remains unclear. In this study, we investigated the effects of aurora kinase A onPKC-induced cell invasion, migration, and EMT in human SW480colon cancer cells. Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) changed the expression levels of EMT markers,increasing α-SMA, vimentin, and MMP-9 expression and decreasingE-cadherin expression, with changes in cell morphology. TPA treatment induced EMT in a PKC-dependent manner. Moreover,the inhibition of aurora kinase A by siRNAs and inhibitors(reversine and VX-680) suppressed TPA-induced cell invasion,migration, and EMT in SW480 human colon cells. Inhibition ofaurora kinase A blocked TPA-induced vimentin and MMP-9 expression,and decreased E-cadherin expression. Furthermore, theknockdown of aurora kinase A decreased the transcriptionalactivity of NF-κB and AP-1 in PKC-stimulated SW480 cells. Thesefindings indicate that aurora kinase A induces migration andinvasion by inducing EMT in SW480 colon cancer cells. To thebest of our knowledge, this is the first study that showed aurorakinase A is a key molecule in PKC-induced metastasis in coloncancer cells.
Lee, Young-Rae,Yu, Hong-Nu,Noh, Eun-Mi,Kim, Jong-Suk,Song, Eun-Kyung,Han, Myung-Kwan,Kim, Byeong-Soo,Lee, Sung-Ho,Park, Jinny Elsevier Science Publishers 2007 INTERNATIONAL JOURNAL OF HEMATOLOGY Vol.85 No.3
<P>Peroxisome proliferator-activated receptor gamma (PPARgamma) and retinoic acid receptors (RARs) have been a focus in chemotherapy for human cancers. The tumor suppressor PTEN plays a pivotal role in the growth of human cancer cells. We investigated whether costimulation of PPARgamma and RAR could synergistically up-regulate PTEN in human leukemia cells and consequently potentiate the inhibition of growth and cell cycle progression of these cells. We found that overexpression of PTEN with the adenoviral vector Ad/PTEN caused growth arrest at the G1 phase of the cell cycle of HL-60 cells. HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand (all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. The 2 compounds in combination showed synergistic effects on PTEN expression at the protein and messenger RNA levels. Moreover, the combination of ciglitazone and ATRA synergistically reduced cell growth rates and cell cycle arrest at the G1 phase. Our results suggest that, PPARgamma and RAR play an important role in controlling the growth of leukemia cells via the up-regulation of PTEN.</P>
TNF-α upregulates PTEN via NF-κB signaling pathways in human leukemic cells
Lee, Young-Rae,Yu, Hong-Nu,Noh, Eun-Mi,Youn, Hyun Jo,Song, Eun-Kyung,Han, Myung-Kwan,Park, Chang-Sik,Kim, Byung-Soo,Park, Young-Seok,Park, Byung-Kwon,Lee, Sung-Ho,Kim, Jong-Suk 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10
TNF-αplays a variety of biological functions such as apoptosis, inflammation and immunity. PTEN also has various cellular function including cell growth, proliferation, migration and differentiation. Thus, possible relationships between the two molecules are suggested. TNF-α has been known to down-regulate PTEN via NF-κB pathway in the human colon cell line, HT-29. However, here we show the opposite finding that TNF-α upregulates PTEN via activation of NF-κB in human leukemic cells. TNF-α increased PTEN expression at HL-60 cells in a time- and dose-dependent manner, but the response was abolished by disruption of NF-κB with p65 anisense phosphorothioate oligonucleotide or pyrrolidine dithiocarbamate. We found that TNF-α activated the NF-κB pathways, evidenced by the translocation of p65 to the nucleus in TNF-α-treated cells. We conclude that TNF-α induces upregulation of PTEN expression through NF-κB activation in human leukemic cells.
Hwang, Jin-Ki,Yu, Hong-Nu,Noh, Eun-Mi,Kim, Jeong-Mi,Hong, On-Yu,Youn, Hyun Jo,Jung, Sung Hoo,Kwon, Kang-Beom,Kim, Jong-Suk,Lee, Young-Rae D.A. Spandidos 2017 Oncology letters Vol.13 No.1
<P>Docosahexaenoic acid (DHA) is an omega-3 fatty acid that is considered to have applications in cancer prevention and treatment. The beneficial effects of DHA against cancer metastasis are well established; however, the mechanisms underlying these effects in breast cancer are not clear. Cell invasion is critical for neoplastic metastasis, and involves the degradation of the extracellular matrix by matrix metalloproteinase (MMP)-9. The present study investigated the inhibitory effect of DHA on MMP-9 expression and cell invasion induced by 12-<I>O</I>-tetradecanoylphorbol-13-acetate (TPA) in the MCF-7 breast cancer cell line. DHA inhibited the TPA-induced activation of mitogen-activated protein kinase (MAPK) and the transcription of nuclear factor (NF)-κB, but did not inhibit the transcription of activator protein-1. DHA increased the activity of peroxisome proliferator-activated receptor (PPAR)-γ, an effect that was reversed by the application of the PPAR-γ antagonist GW9662. In addition, combined treatment with GW9662 and DHA increased NF-κB-related protein expression. These results indicate that DHA regulates MMP-9 expression and cell invasion via modulation of the MAPK signaling pathway and PPAR-γ/NF-κB activity. This suggests that DHA could be a potential therapeutic agent for the prevention of breast cancer metastasis.</P>
Silibinin Enhances Ultraviolet B-Induced Apoptosis in MCF-7 Human Breast Cancer Cells
노은미,Mi Suk Yi,윤현조,Byoung Kil Lee,이영래,Ji-Hey Han,Hong-Nu Yu,김종석,정성후 한국유방암학회 2011 Journal of breast cancer Vol.14 No.1
Purpose: Chemotherapies for breast cancer generally have strong cellular cytotoxicity and severe side effects. Thus, significant emphasis has been placed on combinations of naturally occurring chemopreventive agents. Silibinin is a major bioactive flavonolignan extracted from milk thistle with chemopreventive activity in various organs including the skin, prostate, and breast. However, the mechanism underlying the inhibitory action of silibinin in breast cancer has not been completely elucidated. Therefore, we investigated the effect of silibinin in MCF-7 human breast cancer cells and determined whether silibinin enhances ultraviolet (UV) B-induced apoptosis. Methods: The effects of silibinin on MCF-7 cell viability were determined using the MTT assay. The effect of silibinin on PARP cleavage, as the hallmark of apoptotic cell death, and p53 protein expression in MCF-7 cells was analyzed using Western blot. The effect of silibinin on UVB-induced apoptosis in MCF-7 cells was analyzed by flow cytometry. Results: A dose- and time-dependent reduction in viability was observed in MCF-7 cells treated with silibinin. Silibinin strongly induced apoptotic cell death in MCF-7 cells, and induction of apoptosis was associated with increased p53 expression. Moreover, silibinin enhanced UVB- induced apoptosis in MCF-7 cells. Conclusion: Silibinin induced a loss of cell viability and apoptotic cell death in MCF-7 cells. Furthermore, the combination of silibinin and UVB resulted in an additive effect on apoptosis in MCF-7 cells. These results suggest that silibinin might be an important supplemental agent for treating patients with breast cancer.