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  • 1
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    Online Resource
    Phosphoglycerate kinase 1‐overexpressing lung cancer cells reduce cyclooxygenase 2 expression and promote anti‐tumor immunity in vivo
    Wiley ; 2008
    In:  International Journal of Cancer Vol. 123, No. 12 ( 2008-12-15), p. 2840-2848
    Details
    In: International Journal of Cancer, Wiley, Vol. 123, No. 12 ( 2008-12-15), p. 2840-2848
    Abstract: In addition to the known function in the glycolytic pathway, phosphoglycerate kinase 1 (PGK‐1) promotes reduction of plasmin disulfide bonds leading to angiostatin formation and inhibition of tumor angiogenesis. In this study, the effects of PGK‐1 on anti‐ tumor immunity against lung cancer were evaluated using the Tet‐Off control of PGK‐1 expression in the Lewis lung carcinoma (LLC‐1). There was no significant difference in cell proliferation between parental LLC‐1 and LLC‐1 transduced with PGK‐1 (PGK‐LLC‐1). However, expression of PGK‐1 was found to limit tumor growth in mice subcutaneously injected with the cell lines and tumor growth was restored after doxycycline treatment. In addition, the cell invasion ability of PGK‐LLC‐1 became weaker than that of LLC‐1. Expressions of COX‐2, TGF‐β1 and PGE2 were all found to be down‐regulated in PGK‐LLC‐1. PGK‐LLC‐1 cells treated with doxycycline recovered their COX‐2 protein expression. In the presence of conditioned medium from PGK‐LLC‐1, the endothelial cell migration was reduced. Moreover, PGK‐LLC‐1 also stimulated T lymphocytes to express higher levels of Th1 cytokine (IFN‐γ) and lower levels of IL‐10 in comparison with parental LLC‐1. PGK‐LLC‐1 cells restored the growth rate in immunodeficient mice when compared with the growth rate in normal mice. In the tissue sections, reduced COX‐2 expressions and marked infiltrated CD3 T lymphocytes were observed in the PGK‐LLC‐1 injected group. These findings indicate that overexpression of PGK‐1 in LLC‐1 reduces the COX‐2 expression, and, in turn, affect PGE2, cell invasion, angiogenesis, and the immune functions, and finally inhibit the tumor progression. © 2008 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v123:12
    DOI: 10.1002/ijc.23888
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 2
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    Online Resource
    Cold‐induced ependymin expression in zebrafish and carp brain: implications for cold acclimation
    Wiley ; 1999
    In:  FEBS Letters Vol. 459, No. 1 ( 1999-10), p. 95-99
    Details
    In: FEBS Letters, Wiley, Vol. 459, No. 1 ( 1999-10), p. 95-99
    Abstract: Cold acclimation has been suggested to be mediated by alternations in the gene expression pattern in the cold‐adapted fish. To investigate the mechanism of cold acclimation in fish brain at the molecular level, relevant subsets of differentially expressed genes of interest were identified and cloned by the PCR‐based subtraction suppression hybridization. Characterization of the selected cold‐induced cDNA clones revealed one encoding ependymin. This gene was shown to be brain‐specific. The expression of ependymin was induced by a temperature shift from 25°C to 6°C in Cyprinus carpio or 12°C in Danio rerio . Activation of ependymin was detected 2 h after cold exposure and peaked at more than 10‐fold at 12 h. This peak level remains unchanged until the temperature returns to 25°C. Although the amount of soluble ependymin protein in brain was not changed by cold treatment, its level in the fibrous insoluble polymers increased 2‐fold after exposure to low temperature. These findings indicate that the increase in ependymin expression is an early event that may play an important role in the cold acclimation of fish.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Article
    DOI: 10.1016/S0014-5793(99)01229-6
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 1999
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 3
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    Online Resource
    Emodin modulates epigenetic modifications and suppresses bladder carcinoma cell growth
    Wiley ; 2015
    In:  Molecular Carcinogenesis Vol. 54, No. 3 ( 2015-03), p. 167-177
    Details
    In: Molecular Carcinogenesis, Wiley, Vol. 54, No. 3 ( 2015-03), p. 167-177
    Abstract: The deregulation of epigenetics was involved in early and subsequent carcinogenic events. Reversing cancer epigenetics to restore a normal epigenetic condition could be a rational approach for cancer treatment and specialized prevention. In the present study, we found that the expression levels of two epigenetic markers, histone H3K27 trimethylation (H3K27me3), was low but histone H3S10 phosphorylation (pH3Ser10) was high in human bladder cancer tissues, which showed opposite expression patterns in their normal counterparts. Thus, we investigated whether a natural product, emodin, has the ability to reverse these two epigenetic modifications and inhibit bladder cancer cell growth. Emodin significantly inhibited the cell growth of four bladder cancer cell lines in a dose‐ and time‐dependent manner. Emodin treatment did not induce specific cell cycle arrest, but it altered epigenetic modifications. Emodin treatment resulted in the suppression of pH3Ser10 and increased H3K27me3, contributing to gene silencing in bladder cancer cells. Microarray analysis demonstrated that oncogenic genes including fatty acid binding protein 4 (FABP4) and fibroblast growth factor binding protein 1 (HBP17), RGS4, tissue inhibitor of metalloproteinase 3 (TIMP3), WNT5b, URB, and collagen, type VIII, alpha 1 (COL8A1) responsible for proliferation, survival, inflammation, and carcinogenesis were significantly repressed by emodin. The ChIP assays also showed that emodin increased H3K27me3 but decreased pH3Ser10 modifications on the promoters of repressed genes, which indicate that emodin reverses the cancer epigenetics towards normal epigenetic situations. In conclusion, our work demonstrates the significant anti‐neoplastic activity of emodin on bladder cancer cells and elucidates the novel mechanisms of emodin‐mediated epigenetic modulation of target genes. Our study warrants further investigation of emodin as an effective therapeutic or preventive agent for bladder cancer. © 2013 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    URL: Article
    DOI: 10.1002/mc.v54.3
    DOI: 10.1002/mc.22084
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2001984-1
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  • 4
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    Online Resource
    Platinum‐based combination chemotherapy triggers cancer cell death through induction of BNIP3 and ROS, but not autophagy
    Wiley ; 2020
    In:  Journal of Cellular and Molecular Medicine Vol. 24, No. 2 ( 2020-01), p. 1993-2003
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 24, No. 2 ( 2020-01), p. 1993-2003
    Abstract: These days, cancer can still not be effectively cured because cancer cells readily develop resistance to anticancer drugs. Therefore, an effective combination of drugs with different mechanisms to prevent drug resistance has become a very important issue. Furthermore, the BH3‐only protein BNIP3 is involved in both apoptotic and autophagic cell death. In this study, lung cancer cells were treated with a chemotherapy drug alone or in combination to identify the role of BNIP3 and autophagy in combination chemotherapy for treating cancer. Our data revealed that various combinational treatments of two drugs could increase cancer cell death and cisplatin in combination with rapamycin or LBH589, which triggered the cell cycle arrest at the S phase. Cells with autophagosome and pEGFP‐LC3 puncta increased when treated with drugs. To confirm the role of autophagy, cancer cells were pre‐treated with the autophagy inhibitor 3‐methyladenine (3‐MA). 3‐MA sensitized cancer cells to chemotherapy drug treatments. These results suggest that autophagy may be responsible for cell survival in combination chemotherapy for lung cancer. Moreover, BNIP3 was induced and localized in mitochondria when cells were treated with drugs. The transfection of a dominant negative transmembrane deletion construct of BNIP3 (BNIP3ΔTM) and treatment of a reactive oxygen species (ROS) inhibitor suppressed chemo drug‐induced cell death. These results indicate that BNIP3 and ROS may be involved in combination chemo drug‐induced cell death. However, chemo drug‐induced autophagy may protect cancer cells from drug cytotoxicity. As a result, inhibiting autophagy may improve the effects of combination chemotherapy when treating lung cancer.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.v24.2
    DOI: 10.1111/jcmm.14898
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2076114-4
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  • 5
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    Galectin‐3 promotes CXCR 2 to augment the stem‐like property of renal cell carcinoma
    Wiley ; 2018
    In:  Journal of Cellular and Molecular Medicine Vol. 22, No. 12 ( 2018-12), p. 5909-5918
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 22, No. 12 ( 2018-12), p. 5909-5918
    Abstract: Although targeted therapy is usually the first‐line treatment for advanced renal cell carcinoma ( RCC ), some patients can experience drug resistance. Cancer stem cells are tumour‐initiating cells that play a vital role in drug resistance, metastasis and cancer relapse, while galectins (Gal) participate in tumour progression and drug resistance. However, the exact role of galectins in RCC stemness is yet unknown. In this study, we grew a subpopulation of RCC cells as tumour spheres with higher levels of stemness‐related genes, such as Oct4, Sox2 and Nanog. Among the Gal family, Gal‐3 in particular was highly expressed in RCC tumour spheres. To further investigate Gal‐3's role in the stemness of RCC , lentivirus‐mediated knockdown and overexpression of Gal‐3 in RCC cells were used to examine both in vitro and in vivo tumorigenicity. We further assessed Gal‐3 expression in RCC tissue microarray using immunohistochemistry. Upon suppressing Gal‐3 in parental RCC cells, invasion, colony formation, sphere‐forming ability, drug resistance and stemness‐related gene expression were all significantly decreased. Furthermore, CXCL 6, CXCL 7 and CXCR 2 were down‐regulated in Gal‐3‐knockdown tumour spheres, while CXCR 2 overexpression in Gal‐3‐knockdown RCC restored the ability of sphere formation. Gal‐3 overexpression in RCC promoted both in vitro and in vivo tumorigenicity, and its expression was correlated with CXCR 2 expression and tumour progression in clinical tissues. RCC patients with higher co‐expressions of Gal‐3 and CXCR 2 demonstrated a worse survival rate. These results indicate that highly expressed Gal‐3 may up‐regulate  CXCR 2 to augment RCC stemness. Gal‐3 may be a prognostic and innovative target of combined therapy for treating RCC .
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2018.22.issue-12
    DOI: 10.1111/jcmm.13860
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2076114-4
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  • 6
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    Arginines in the CDR of anti‐dsDNA autoantibodies facilitate cell internalization via electrostatic interactions
    Wiley ; 2008
    In:  European Journal of Immunology Vol. 38, No. 11 ( 2008-11), p. 3178-3190
    Details
    In: European Journal of Immunology, Wiley, Vol. 38, No. 11 ( 2008-11), p. 3178-3190
    Abstract: Internalization of autoantibodies against double‐stranded DNA (anti‐dsDNA) is crucial to the pathogenesis of systemic lupus erythematosus. Anti‐dsDNA may bind to cell‐surface targets in order to facilitate the subsequent cell penetration of the anti‐dsDNA. In this study, we observed that the 9D7 monoclonal anti‐dsDNA autoantibody (9D7 mAb) penetrates into Jurkat cells via a novel alternative pathway. Endocytosis inhibitors or a lipid‐raft inhibitor did not significantly change the penetration of 9D7 mAb into the Jurkat cells. However, heparin sulfate, chondroitin sulfate B, decaarginine and chondroitinase ABC significantly suppressed the internalization and the 9D7 mAb inhibited the internalization of Tat‐GFP. Moreover, the penetration of the 9D7 mAb was significantly reduced in proteoglycan‐deficient cells (pgs A‐745). Positively charged amino acids including arginine are commonly found in the CDR of the 9D7 mAb. Point mutations to the arginine residues in the CDR of the H chain of the recombinant 9D7 mAb significantly attenuated its DNA‐binding and cell‐penetration abilities. These findings indicate that cell penetration of anti‐dsDNA is due to the electrostatic interactions of arginine residues in the CDR with the negatively charged sulfated polysaccharides on the cell surface.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v38:11
    DOI: 10.1002/eji.200838678
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 1491907-2
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  • 7
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    Online Resource
    The relationship between varicoceles and obesity in a young adult population
    Wiley ; 2009
    In:  International Journal of Andrology Vol. 32, No. 4 ( 2009-08), p. 385-390
    Details
    In: International Journal of Andrology, Wiley, Vol. 32, No. 4 ( 2009-08), p. 385-390
    Type of Medium: Online Resource
    ISSN: 0105-6263 , 1365-2605
    URL: Issue
    URL: Article
    DOI: 10.1111/ija.2009.32.issue-4
    DOI: 10.1111/j.1365-2605.2008.00926.x
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2011828-4
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  • 8
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    Online Resource
    Combination of Fasl and GM‐CSF confers synergistic antitumor immunity in an in vivo model of the murine Lewis lung carcinoma
    Wiley ; 2008
    In:  International Journal of Cancer Vol. 123, No. 1 ( 2008-07), p. 123-133
    Details
    In: International Journal of Cancer, Wiley, Vol. 123, No. 1 ( 2008-07), p. 123-133
    Abstract: Gene transfer of Fas ligand (FasL) to tumor cells has been demonstrated to inhibit tumor growth in vivo , and neutrophils are primarily responsible for this immunoprotection. The granulocyte–macrophage colony stimulating factor (GM‐CSF) secreted by tumor vaccine can recruit dendritic cells (DCs) for efficient antigen presentation to T cells that generate the tumor‐specific response. To investigate whether the combination of FasL and GM‐CSF can efficiently suppress tumor growth, we have established Lewis lung carcinoma (LLC‐1) cells that are transduced with GM‐CSF (LLC/GM‐CSF), FasL (LLC/FasL) or both genes (LLC/FasL/GM‐CSF) to test their tumorigenic potential in vivo . Mice inoculated with LLC/GM‐CSF display high survival rates along with reduction of tumor growth. In contrast, none of the mice injected with LLC/FasL or LLC/FasL/GM‐CSF develop tumors. Specific memory immune response and delayed LLC‐1 tumor growth are found in mice immunized with LLC‐1/FasL or LLC‐1/FasL/GM‐CSF. Furthermore, therapeutic effects are observed only when LLC‐1/FasL/GM‐CSF tumor vaccine is employed to retard growth of preexisting LLC‐1 tumors. Tumor growth is also completely suppressed in mice injected with a mixture of LLC‐1 and LLC‐1/FasL/GM‐CSF. In addition, IL‐12 production, cytotoxic T‐cell activity and IgG against LLC‐1 are manifested in mice injected with LLC/FasL/GM‐CSF. Our data show that FasL‐induced pathway triggers expression of proinflammatory cytokines, including IL‐1β, IL‐6, MIP‐2 and MCP‐1, while GM‐CSF‐dependent pathway promotes functional maturation and activation of DCs. Taken together, the results indicate that dual gene‐based delivery with FasL and GM‐CSF may serve as a more effective tumor vaccine to suppress lung cancer cell growth in vivo . © 2008 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v123:1
    DOI: 10.1002/ijc.23474
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 9
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    Online Resource
    The effect of circumcision on young adult sexual function
    Wiley ; 2014
    In:  The Kaohsiung Journal of Medical Sciences Vol. 30, No. 6 ( 2014-06), p. 305-309
    Details
    In: The Kaohsiung Journal of Medical Sciences, Wiley, Vol. 30, No. 6 ( 2014-06), p. 305-309
    Abstract: Whether sexual function is affected by circumcision is a subject of considerable debate among advocate and opponent opinions. We analyzed the sexual function of young men, and the differences between those who were uncircumcised and circumcised, in Taiwan. A total of 506 patients who received circumcision between January 2009 and March 2011 at the urology department in our center were enrolled. Before circumcision, the patients' sexual performances were evaluated using the International Index of Erectile Function‐5 (IIEF‐5), and the Brief Male Sexual Function Inventory (BMSFI) questionnaires. They were evaluated using the questionnaires again, after a postoperative interval of 90 days. Furthermore, intravaginal ejaculation latency times (IELT) of the patients were also measured. The IELT and scores in five main domains of the BMSFI, and IIEF, before and after circumcision, were analyzed. A total of 442 patients were available for follow up. The mean age was 25.14 ± 4.46 years (range = 19–35 years). The differences in the BMSFI scores were statistically significant ( p   〈  0.001), especially in increasing sex drive after circumcision ( p   〈  0.001). The IIEF‐5 score showed no statistically difference before and after circumcision ( p  = 0.141). However, after the circumcision, the participants had more erection confidence ( p   〈  0.001), more difficulty in maintaining erections in completing intercourse ( p  = 0.01), and showed lower IELT scores ( p  = 0.06). The sexual performance, especially with regards to sex drive and mental erection confidence, seemed to have improved among the patients after circumcision. Our findings may help urologists to better counsel young men receiving circumcisions.
    Type of Medium: Online Resource
    ISSN: 1607-551X , 2410-8650
    URL: Article
    DOI: 10.1016/j.kjms.2013.10.004
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2202782-8
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  • 10
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    Online Resource
    CEA‐producing urothelial cell carcinoma with metastasis presenting as a rectal adenocarcinoma
    Wiley ; 2012
    In:  The Kaohsiung Journal of Medical Sciences Vol. 28, No. 11 ( 2012-11), p. 624-627
    Details
    In: The Kaohsiung Journal of Medical Sciences, Wiley, Vol. 28, No. 11 ( 2012-11), p. 624-627
    Abstract: This is a case study of a 61‐year‐old male who presented with difficult defecation for 1 month. A circumferential submucosal rectal tumor was noted on a digital rectal examination and colonoscopy. Laboratory examination revealed high serum levels of carcinoembryonic antigen (CEA; 43.75 ng/mL) and carbohydrate antigen 19‐9 (CA19‐9; 11,790 U/mL). In addition, tumor biopsies revealed a poorly differentiated adenocarcinoma of the rectum with intact mucosa. The patient had history of advanced stage‐T2 urothelial cell carcinoma of bladder, which had been downstaged to T0 by neoadjuvant chemotherapy followed by radical cystectomy 1 year prior. After investigating the initial bladder tumor specimens, a small portion of the tumor with high CEA expression comparable to the submucosal rectal tumor was found. The size of the tumor was reduced and the levels of the tumor markers decreased after administering FOLFIRI chemotherapy targeted at the adenocarcinoma. Although neoadjuvant chemotherapy may have a selective pressure to eliminate most urothelial cell carcinoma, physicians should be aware that it can lead to rectal metastasis via CEA‐producing components.
    Type of Medium: Online Resource
    ISSN: 1607-551X , 2410-8650
    URL: Article
    DOI: 10.1016/j.kjms.2012.04.030
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2202782-8
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