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  1. Article ; Online: Comparing the bond strength of fiber post cementation in the root canal using pre- and co-curing procedures with the same self-etching bonding system.

    Chou, I-Chian / Wang, Hao-Ting / Chen, Yung-Chung / Hsu, Yi-Fan / He, Wei-Hung

    Journal of dental sciences

    2022  Volume 17, Issue 4, Page(s) 1689–1696

    Abstract: Background/purpose: Self-etching bonding systems are widely used in fiber post cementation. However, no clear guidelines are established for choosing pre- or co-curing procedures. We investigated the bond strength of fiber post cementation using pre-/co- ...

    Abstract Background/purpose: Self-etching bonding systems are widely used in fiber post cementation. However, no clear guidelines are established for choosing pre- or co-curing procedures. We investigated the bond strength of fiber post cementation using pre-/co-curing methods in self-etching bonding systems and compared them with those of a self-adhesive system.
    Materials and methods: Post spaces were prepared in 30 single-rooted premolars/canines, and the fiber posts were cemented in three ways (10 specimens per group): using a self-etching bonding system with either a pre-curing or simultaneous co-curing procedure (RelyX™ Ultimate; groups SE-pre and SE-co, respectively) and using a self-adhesive system (RelyX™ Unicem 2, group SA). Each specimen was embedded and sliced perpendicularly to the long axis into three 2.5-mm-thick sections. Microphotographs of the coronal and apical surfaces of each section were acquired, and push-out tests (1 mm/min) were performed. One-way analysis of variance was conducted on the data, followed by Tukey's honestly significant difference post hoc test.
    Results: The bond strength in the whole root was not significantly different among the three groups. When independently evaluating each portion, group SE-co exhibited significantly lower coronal bond strength. The bond strength varied among root regions only in group SE-pre; the apical region had a significantly lower value.
    Conclusion: No cementation method is superior in all portions. Regarding pre-curing methods, clinicians must caution the fit between the post and post space, which may be affected by the pre-polymerized bond layer. The co-curing method used in a larger coronal cement space contributes to the poor bond strength.
    Language English
    Publishing date 2022-03-17
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2213-8862
    ISSN (online) 2213-8862
    DOI 10.1016/j.jds.2022.02.016
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  2. Article: Traditional Chinese Medicine in Patients With Primary Sjogren's Syndrome: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

    Chen, Huang-Hsi / Lai, Jung-Nien / Yu, Min-Chien / Chen, Chia-Yin / Hsieh, Yi-Ting / Hsu, Yi-Fan / Wei, James Cheng-Chung

    Frontiers in medicine

    2021  Volume 8, Page(s) 744194

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2021-09-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2021.744194
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  3. Article ; Online: Low-Dose Nicotine Activates EGFR Signaling via α5-nAChR and Promotes Lung Adenocarcinoma Progression.

    Wang, Mong-Lien / Hsu, Yi-Fan / Liu, Chih-Hsuan / Kuo, Ya-Ling / Chen, Yi-Chen / Yeh, Yi-Chen / Ho, Hsiang-Ling / Wu, Yu-Chung / Chou, Teh-Ying / Wu, Cheng-Wen

    International journal of molecular sciences

    2020  Volume 21, Issue 18

    Abstract: Nicotine in tobacco smoke is considered carcinogenic in several malignancies including lung cancer. The high incidence of lung adenocarcinoma (LAC) in non-smokers, however, remains unexplained. Although LAC has long been less associated with smoking ... ...

    Abstract Nicotine in tobacco smoke is considered carcinogenic in several malignancies including lung cancer. The high incidence of lung adenocarcinoma (LAC) in non-smokers, however, remains unexplained. Although LAC has long been less associated with smoking behavior based on previous epidemiological correlation studies, the effect of environmental smoke contributing to low-dose nicotine exposure in non-smoking population could be underestimated. Here we provide experimental evidence of how low-dose nicotine promotes LAC growth in vitro and in vivo. Screening of nicotinic acetylcholine receptor subunits in lung cancer cell lines demonstrated a particularly high expression level of nicotinic acetylcholine receptor subunit α5 (α 5-nAChR) in LAC cell lines. Clinical specimen analysis revealed up-regulation of α 5-nAChR in LAC tumor tissues compared to non-tumor counterparts. In LAC cell lines α 5-nAChR interacts with epidermal growth factor receptor (EGFR), positively regulates EGFR pathway, enhances the expression of epithelial-mesenchymal transition markers, and is essential for low-dose nicotine-induced EGFR phosphorylation. Functionally, low-dose nicotine requires α 5-nAChR to enhance cell migration, invasion, and proliferation. Knockdown of α 5-nAChR inhibits the xenograft tumor growth of LAC. Clinical analysis indicated that high level of tumor α 5-nAChR is correlated with poor survival rates of LAC patients, particularly in those expressing wild-type EGFR. Our data identified α 5-nAChR as an essential mediator for low-dose nicotine-dependent LAC progression possibly through signaling crosstalk with EGFR, supporting the involvement of environmental smoke in tumor progression in LAC patients.
    MeSH term(s) Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/mortality ; Adenocarcinoma of Lung/pathology ; Animals ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/genetics ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Disease Progression ; Epithelial-Mesenchymal Transition/drug effects ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/genetics ; Gene Knockdown Techniques ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/mortality ; Lung Neoplasms/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/metabolism ; Nicotine/toxicity ; Phosphorylation ; Receptors, Nicotinic/genetics ; Receptors, Nicotinic/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Tobacco Smoke Pollution/adverse effects ; Up-Regulation/drug effects ; Xenograft Model Antitumor Assays
    Chemical Substances Receptors, Nicotinic ; Tobacco Smoke Pollution ; Nicotine (6M3C89ZY6R) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2020-09-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21186829
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  4. Article ; Online: Stimulation of Proliferation and Migration of Mouse Macrophages by Type B CpG-ODNs Is F-Spondin and IL-1Ra Dependent.

    Chen, Tai-An / Liao, Chiao-Chun / Cheng, Yung-Chih / Chen, Yen-Po / Hsu, Yi-Fan / Liang, Chi-Ming / Liang, Shu-Mei

    PloS one

    2015  Volume 10, Issue 6, Page(s) e0128926

    Abstract: Macrophage proliferation and migration are important for many facets of immune response. Here we showed that stimulation of macrophages with type B CpG oligodeoxynucleotides (CpG-B ODNs) such as CpG-ODN 1668 increased the production of anti-inflammatory ... ...

    Abstract Macrophage proliferation and migration are important for many facets of immune response. Here we showed that stimulation of macrophages with type B CpG oligodeoxynucleotides (CpG-B ODNs) such as CpG-ODN 1668 increased the production of anti-inflammatory cytokine interleukin 1 receptor antagonist (IL-1Ra) in a TLR9- and MyD88-dependent manner. The CpG-B ODNs-induced IL-1Ra increased macrophage migration and promoted macrophage proliferation by down-regulating the expression of a cell cycle negative regulator, p27 to increase cell population in the S phase. The induction of IL-1Ra by CpG-B ODNs was F-spondin dependent. Knockdown of F-spondin and IL-1Ra decreased CpG-B ODNs-induced macrophage migration whereas overexpression of IL-1Ra increased migration of those cells. These findings demonstrated novel roles for F-spondin and IL-1Ra in CpG-B ODNs-mediated cell proliferation and migration of macrophages.
    MeSH term(s) Animals ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Extracellular Matrix Proteins/metabolism ; Gene Knockdown Techniques ; Interleukin 1 Receptor Antagonist Protein/metabolism ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/metabolism ; Mice ; Mice, Inbred BALB C ; Myeloid Differentiation Factor 88/metabolism ; Oligodeoxyribonucleotides/pharmacology ; RAW 264.7 Cells ; S Phase/drug effects ; Signal Transduction/drug effects ; Toll-Like Receptor 9/metabolism ; Up-Regulation/drug effects
    Chemical Substances CPG-oligonucleotide ; Extracellular Matrix Proteins ; F-spondin protein, mouse ; Interleukin 1 Receptor Antagonist Protein ; Myeloid Differentiation Factor 88 ; Oligodeoxyribonucleotides ; Toll-Like Receptor 9
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0128926
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  5. Article ; Online: Complement activation mediates cetuximab inhibition of non-small cell lung cancer tumor growth in vivo

    Gurpide Alfonso / Lopez-Picazo Jose M / Corrales Leticia / Ajona Daniel / Hsu Yi-Fan / Montuenga Luis M / Pio Ruben

    Molecular Cancer, Vol 9, Iss 1, p

    2010  Volume 139

    Abstract: Abstract Background Cetuximab, an antibody targeting the epidermal growth factor receptor (EGFR), increases survival in patients with advanced EGFR-positive non-small cell lung cancer when administrated in combination with chemotherapy. In this study, we ...

    Abstract Abstract Background Cetuximab, an antibody targeting the epidermal growth factor receptor (EGFR), increases survival in patients with advanced EGFR-positive non-small cell lung cancer when administrated in combination with chemotherapy. In this study, we investigated the role of complement activation in the antitumor mechanism of this therapeutic drug. Results EGFR-expressing lung cancer cell lines were able to bind cetuximab and initiate complement activation by the classical pathway, irrespective of the mutational status of EGFR. This activation led to deposition of complement components and increase in complement-mediated cell death. The influence of complement activation on the activity of cetuximab in vivo was evaluated in xenografts of A549 lung cancer cells on nude mice. A549 cells express wild-type EGFR and have a KRAS mutation. Cetuximab activity against A549 xenografts was highly dependent on complement activation, since complement depletion completely abrogated the antitumor efficacy of cetuximab. Moreover, cetuximab activity was significantly higher on A549 cells in which a complement inhibitor, factor H, was genetically downregulated. Conclusions We demonstrate for the first time that the in vivo antitumor activity of cetuximab can be associated with a complement-mediated immune response. These results may have important implications for the development of new cetuximab-based therapeutic strategies and for the identification of markers that predict clinical response.
    Keywords Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Subject code 616 ; 610
    Language English
    Publishing date 2010-06-01T00:00:00Z
    Publisher BioMed Central
    Document type Article ; Online
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  6. Article: Non-small cell lung cancer cells produce a functional set of complement factor I and its soluble cofactors.

    Okroj, Marcin / Hsu, Yi-Fan / Ajona, Daniel / Pio, Ruben / Blom, Anna M

    Molecular immunology

    2008  Volume 45, Issue 1, Page(s) 169–179

    Abstract: The complement system is important for protection from invading pathogens, removal of waste products and guidance of the immune response. Furthermore, complement can be also targeted to cancer cells. However, membrane-bound inhibitors over-expressed by ... ...

    Abstract The complement system is important for protection from invading pathogens, removal of waste products and guidance of the immune response. Furthermore, complement can be also targeted to cancer cells. However, membrane-bound inhibitors over-expressed by certain types of tumor cells restrict the cytotoxic activity of complement. Herein we report that non-small cell lung cancer (NSCLC) cells produce soluble complement inhibitors factor I (FI) and C4b-binding protein (C4BP). FI is a serine protease capable of degrading the activated complement components C3b and C4b, whilst C4BP acts as its cofactor. Furthermore, NSCLC cells express membrane-bound regulators and shed membrane cofactor protein (MCP), which shares cofactor function with C4BP. Secretion of FI from NSCLC cells was higher than previously reported for any non-hepatic source and FI produced by these cells could efficiently support cleavage of C3b and C4b. In vitro functional assays revealed that additional FI significantly decreased C3 deposition and complement-dependent lysis, particularly when cofactors were added. Our results demonstrate that soluble inhibitors produced by NSCLC cells may provide further protection from complement beyond the level ensured by membrane-bound inhibitors and, as such, contribute to the aggressive phenotype of these lung cancer cells.
    MeSH term(s) Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/immunology ; Cell Line, Tumor ; Complement Activation/immunology ; Complement C3b/metabolism ; Complement C4b/metabolism ; Complement C4b-Binding Protein ; Complement Factor I/biosynthesis ; Complement Factor I/genetics ; Cytotoxicity, Immunologic ; Gene Expression Regulation, Neoplastic ; Histocompatibility Antigens/biosynthesis ; Histocompatibility Antigens/genetics ; Histocompatibility Antigens/metabolism ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/immunology ; Protein Binding ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Solubility
    Chemical Substances C4BPA protein, human ; Complement C4b-Binding Protein ; Histocompatibility Antigens ; RNA, Messenger ; Complement C3b (80295-43-8) ; Complement C4b (80295-50-7) ; Complement Factor I (EC 3.4.21.45)
    Language English
    Publishing date 2008-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 424427-8
    ISSN 1872-9142 ; 0161-5890
    ISSN (online) 1872-9142
    ISSN 0161-5890
    DOI 10.1016/j.molimm.2007.04.025
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  7. Article: Down-regulation of human complement factor H sensitizes non-small cell lung cancer cells to complement attack and reduces in vivo tumor growth.

    Ajona, Daniel / Hsu, Yi-Fan / Corrales, Leticia / Montuenga, Luis M / Pio, Ruben

    Journal of immunology (Baltimore, Md. : 1950)

    2007  Volume 178, Issue 9, Page(s) 5991–5998

    Abstract: Malignant cells are often resistant to complement activation through the enhanced expression of complement inhibitors. In this work, we examined the protective role of factor H, CD46, CD55, and CD59 in two non-small cell lung cancer cell lines, H1264 and ...

    Abstract Malignant cells are often resistant to complement activation through the enhanced expression of complement inhibitors. In this work, we examined the protective role of factor H, CD46, CD55, and CD59 in two non-small cell lung cancer cell lines, H1264 and A549, upon activation of the classical pathway of complement. Complement was activated with polyclonal Abs raised against each cell line. After blocking factor H activity with a neutralizing Ab, C3 deposition and C5a release were more efficient. Besides, a combined inhibition of factor H and CD59 significantly increased complement-mediated lysis. CD46 and CD55 did not show any effect in the control of complement activation. Factor H expression was knockdown on A549 cells using small interfering RNA. In vivo growth of factor H-deficient cells in athymic mice was significantly reduced. C3 immunocytochemistry on explanted xenografts showed an enhanced activation of complement in these cells. Besides, when mice were depleted of complement with cobra venom factor, growth was recovered, providing further evidence that complement was important in the reduction of in vivo growth. In conclusion, we show that expression of the complement inhibitor factor H by lung cancer cells can prevent complement activation and improve tumor development in vivo. This may have important consequences in the efficiency of complement-mediated immunotherapies.
    MeSH term(s) Animals ; CD55 Antigens/drug effects ; CD55 Antigens/immunology ; CD59 Antigens/drug effects ; CD59 Antigens/immunology ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/immunology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Complement Activation/genetics ; Complement C3/analysis ; Complement C3/immunology ; Complement C5a/immunology ; Complement Factor H/antagonists & inhibitors ; Complement Factor H/genetics ; Complement Factor H/immunology ; Cytotoxicity, Immunologic ; Down-Regulation ; Humans ; Immunohistochemistry ; Lung Neoplasms/genetics ; Lung Neoplasms/immunology ; Membrane Cofactor Protein/antagonists & inhibitors ; Membrane Cofactor Protein/immunology ; Mice ; RNA, Small Interfering/pharmacology ; Xenograft Model Antitumor Assays
    Chemical Substances CD55 Antigens ; CD59 Antigens ; Complement C3 ; Membrane Cofactor Protein ; RNA, Small Interfering ; Complement C5a (80295-54-1) ; Complement Factor H (80295-65-4)
    Language English
    Publishing date 2007-03-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.178.9.5991
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    Ud II Zs.37: Show issues Location:
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  8. Article ; Online: Complement activation mediates cetuximab inhibition of non-small cell lung cancer tumor growth in vivo.

    Hsu, Yi-Fan / Ajona, Daniel / Corrales, Leticia / Lopez-Picazo, Jose M / Gurpide, Alfonso / Montuenga, Luis M / Pio, Ruben

    Molecular cancer

    2010  Volume 9, Page(s) 139

    Abstract: Background: Cetuximab, an antibody targeting the epidermal growth factor receptor (EGFR), increases survival in patients with advanced EGFR-positive non-small cell lung cancer when administrated in combination with chemotherapy. In this study, we ... ...

    Abstract Background: Cetuximab, an antibody targeting the epidermal growth factor receptor (EGFR), increases survival in patients with advanced EGFR-positive non-small cell lung cancer when administrated in combination with chemotherapy. In this study, we investigated the role of complement activation in the antitumor mechanism of this therapeutic drug.
    Results: EGFR-expressing lung cancer cell lines were able to bind cetuximab and initiate complement activation by the classical pathway, irrespective of the mutational status of EGFR. This activation led to deposition of complement components and increase in complement-mediated cell death. The influence of complement activation on the activity of cetuximab in vivo was evaluated in xenografts of A549 lung cancer cells on nude mice. A549 cells express wild-type EGFR and have a KRAS mutation. Cetuximab activity against A549 xenografts was highly dependent on complement activation, since complement depletion completely abrogated the antitumor efficacy of cetuximab. Moreover, cetuximab activity was significantly higher on A549 cells in which a complement inhibitor, factor H, was genetically downregulated.
    Conclusions: We demonstrate for the first time that the in vivo antitumor activity of cetuximab can be associated with a complement-mediated immune response. These results may have important implications for the development of new cetuximab-based therapeutic strategies and for the identification of markers that predict clinical response.
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/immunology ; Cell Line, Tumor ; Cetuximab ; Complement Activation/drug effects ; ErbB Receptors/biosynthesis ; ErbB Receptors/genetics ; Female ; Fluorescent Antibody Technique ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/immunology ; Mice ; Mice, Nude ; Mutation ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins p21(ras) ; RNA, Messenger/analysis ; Xenograft Model Antitumor Assays ; ras Proteins/genetics
    Chemical Substances Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; KRAS protein, human ; Proto-Oncogene Proteins ; RNA, Messenger ; ErbB Receptors (EC 2.7.10.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2) ; Cetuximab (PQX0D8J21J)
    Language English
    Publishing date 2010-06-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1476-4598
    ISSN (online) 1476-4598
    DOI 10.1186/1476-4598-9-139
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  9. Article: Involvement of Ras/Raf-1/ERK actions in the magnolol-induced upregulation of p21 and cell-cycle arrest in colon cancer cells.

    Hsu, Yi-Fan / Lee, Tong-Sheng / Lin, Shyr-Yi / Hsu, Sung-Po / Juan, Shu-Hui / Hsu, Yuan-Hsun / Zhong, Wen-Bin / Lee, Wen-Sen

    Molecular carcinogenesis

    2007  Volume 46, Issue 4, Page(s) 275–283

    Abstract: Previously, we showed that magnolol induces cell-cycle arrest in cultured colon and liver cancer cells through an upregulation of the p21 protein. The aim of this study was to delineate the molecular mechanism underlying this magnolol-induced increase of ...

    Abstract Previously, we showed that magnolol induces cell-cycle arrest in cultured colon and liver cancer cells through an upregulation of the p21 protein. The aim of this study was to delineate the molecular mechanism underlying this magnolol-induced increase of p21 protein. Thus our RT-PCR analysis demonstrated that the mRNA levels of p21 were increased at 1 h after magnolol treatment and sustained for at least 24 h. The p21 promoter activity was also increased by magnolol treatment. Western blot analysis demonstrated that treatment of COLO-205 cells with magnolol increased the levels of phosphorylation of extracellular signal-regulated kinase (ERK). Pretreatment of the cells with PD98059 abolished the magnolol-induced upregulation of p21 protein, suggesting the involvement of an ERK pathway in the magnolol-induced upregulation of p21 in COLO-205 cells. Ras inhibitor peptide abolished the magnolol-induced increase of phosphorylated ERK protein levels, increase of p21 protein, and decrease of thymidine incorporation. Moreover, treatment of COLO-205 with magnolol increased the phosphorylated Raf-1 protein (the Ras target molecule). Pretreatment of the cells with Raf-1 inhibitor reversed the magnolol-induced decrease in thymidine incorporation. Treatment of the cells with CaM kinase inhibitor, but not protein kinase A (PKA) inhibitor or phosphatidylinosital 3-kinase (PI3K) inhibitor, abolished the magnolol-induced activation of ERK and decrease of thymidine incorporation. Taken together, our results suggest that magnolol activates ERK phosphorylation through a Ras/Raf-1-mediated pathway. Subsequently, p21 expression is increased, and finally thymidine incorporation is decreased.
    MeSH term(s) Biphenyl Compounds/pharmacology ; Cell Cycle/drug effects ; Cell Line, Tumor ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; Lignans/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-raf/metabolism ; Proto-Oncogene Proteins p21(ras)/metabolism ; Signal Transduction/drug effects ; Up-Regulation/drug effects
    Chemical Substances Biphenyl Compounds ; Lignans ; magnolol (001E35HGVF) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Proto-Oncogene Proteins c-raf (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2007-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1004029-8
    ISSN 1098-2744 ; 0899-1987
    ISSN (online) 1098-2744
    ISSN 0899-1987
    DOI 10.1002/mc.20274
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