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  • 1
    Online Resource
    Online Resource
    Expression of PRDX6 Correlates with Migration and Invasiveness of Colorectal Cancer Cells
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 51, No. 6 ( 2018), p. 2616-2630
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 51, No. 6 ( 2018), p. 2616-2630
    Abstract: Background/Aims: Colorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer-related deaths worldwide. PRDXs are antioxidant enzymes that play an important role in cell differentiation, proliferation and apoptosis and have diverse functions in malignancy development. However, the mechanism of aberrant overexpression of PRDX6 in CRC remains unclear. Methods: Boyden chamber assay, flow cytometry and a lentiviral shRNA targeting PRDX6 and transient transfection with pCMV-6-PRDX6 plasmid were used to examine the role of PRDX6 in the proliferation capacity and invasiveness of CRC cells. Immunohistochemistry (IHC) with tissue array containing 40 paraffin- embedded CRC tissue specimens and Western blot assays were used to detect target proteins. Results: PRDX6 was significantly up-expressed in different comparisons of metastasis of colorectal adenomas in node-positive CRC (P = 0.03). In in vitro HCT-116, PRDX6 silencing markedly suppressed CRC cell migration and invasiveness while also inducing cell cycle arrest as well as the generation of reactive oxygen species (ROS); specific overexpression of PRDX6 had the opposite effect. Mechanistically, the PRDX6 inactivation displayed decreased levels of PRDX6, N-cadherin, β-catenin, Vimentin, Slug, Snail and Twist-1 through the activation of the PI3K/ AKT/p38/p50 pathways, but they were also significantly inhibited by PRDX6 transfectants. There was also increased transcriptional activation of dimethylation of histone H3 lysine 4 (H3K4me3) of PRDX6 promoter via the activation of the PI3K/Akt/NFkB pathways. Conclusion: Our findings demonstrated that PRDX6 expression plays a characteristic growth-promoting role in CRC metastasis. This study suggests that PRDX6 may serve as a biomarker of node-positive status and may have a role as an important endogenous regulator of cancer cell tumorigenicity in CRC. PRDX6 may also be an effective therapeutic target.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000495934
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Quality of Life in Disease-Free Gastric Adenocarcinoma Survivors: Impacts of Clinical Stages and Reconstructive Surgical Procedures
    S. Karger AG ; 2007
    In:  Digestive Surgery Vol. 24, No. 1 ( 2007), p. 59-65
    Details
    In: Digestive Surgery, S. Karger AG, Vol. 24, No. 1 ( 2007), p. 59-65
    Abstract: 〈 i 〉 Aim: 〈 /i 〉 To investigate health-related quality of life data of disease-free gastric adenocarcinoma survivors, with special emphasis on the roles of clinical stages and reconstructive surgical procedures. 〈 i 〉 Methods: 〈 /i 〉 We performed a cross-sectional study in 51 disease-free gastric adenocarcinoma patients. The patients had been followed for at least 6 (median 17, range from 6 months to 2 years) months after initial radical surgery. The Taiwan Chinese version of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Cancer 30 (EORTC QLQ-C30) and the supplementary gastric cancer module QLQ-STO22 were used as outcome measures. 〈 i 〉 Results: 〈 /i 〉 Patients with earlier-/advanced-stage diseases (American Joint Committee on Cancer stages I and II vs. III and IV) had a similar quality of life in terms of global health status and functional and symptomatic well-being. Subtotal gastrectomy outweighed total gastrectomy with better role function and less nausea/vomiting and appetite loss. Multivariate regression analyses also proved that proximal gastric preservation was predictive of better role function, less nausea/vomiting, and less appetite loss. 〈 i 〉 Conclusions: 〈 /i 〉 Gastric adenocarcinoma survivors may enjoy a similar life quality, regardless of their original disease stages. Functional preservation may have marginal advantages to improve patients’ quality of life by reducing symptomatic nausea, vomiting, and appetite loss postoperatively.
    Type of Medium: Online Resource
    ISSN: 0253-4886 , 1421-9883
    URL: Article
    DOI: 10.1159/000100920
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2007
    detail.hit.zdb_id: 1468560-7
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  • 3
    Online Resource
    Online Resource
    Comparative Proteomic Identification of Protein Disulphide Isomerase A6 Associated with Tert-Butylhydroperoxide-Induced Liver Injury in Rat Hepatocytes
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 45, No. 5 ( 2018), p. 1915-1926
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 45, No. 5 ( 2018), p. 1915-1926
    Abstract: Background/Aims: Oxidants are important human toxicants. They have been implicated in the occurrence and development of liver diseases. Increased intracellular tert-butylhydroperoxide (t-BHP) may be critical for oxidant toxicity, and is commonly used for evaluating mechanisms involving oxidative stress, but the method remains controversial. Methods: Primary cultures of hepatocytes as well as human Hep G2 and mouse FL83B liver cells were obtained. Cell viability was measured by annexin V–FITC/propidium iodide and DAPI staining to determine the effects of t-BHP treatment on acute liver injury. A proteomic assay provided information that was used to identify the differentially expressed proteins following t-BHP treatment; immunohistochemistry and western blotting were performed to detect the expression of PDIA6 activity in apoptotic and endoplasmic reticulum (ER) stress pathways. Results: Our results demonstrate that t-BHP treatment of liver cells increased cell cytotoxicity and the generation of reactive oxygen species. This treatment also increased the level of PDIA6; this was validated in vitro and in vivo based on a comparison of t-BHP-treated and -untreated groups. Treatment of mouse liver FL83B cells with t-BHP activated caspase 3, increased the expression of apoptotic molecules, caused cytochrome c release, and induced Bcl-2, Bax and IRE1α/TRAF2 complex formation. t-BHP-dependent induction of apoptosis was accompanied by sustained phosphorylation of the IRE1α/ASK1/JNK1/2/p38 pathways and PDIA6 expression. Furthermore, t-BHP induced liver FL83B cell viability and apoptosis by upregulating the levels of PDIA6; this process could be involved in the activation of the IRE1α/ASK1/JNK1/2/p38 signalling pathways. Conclusions: We conclude that t-BHP induced an apoptosis cascade and ER stress in hepatocytes by upregulation of PDIA6, providing a new mechanism underlying the effects of t-BHP on liver injury.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000487968
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    A Comparative Proteomic Analysis of Erinacine A’s Inhibition of Gastric Cancer Cell Viability and Invasiveness
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 43, No. 1 ( 2017), p. 195-208
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 43, No. 1 ( 2017), p. 195-208
    Abstract: Background / Aims: Erinacine A, isolated from the ethanol extract of the Hericium erinaceus mycelium, has been demonstrated as a new alternative anticancer medicine. Drawing upon current research, this study presents an investigation of the molecular mechanism of erinacine A inhibition associated with gastric cancer cell growth. Methods: Cell viability was determined by Annexin V–FITC/propidium iodide staining and migration using a Boyden chamber assay to determine the effects of erinacine A treatment on the proliferation capacity and invasiveness of gastric cancer cells. A proteomic assay provided information that was used to identify the differentially-expressed proteins following erinacine A treatment, as well as the mechanism of its targets in the apoptotic induction of erinacine A. Results: Our results demonstrate that erinacine A treatment of TSGH 9201 cells increased cytotoxicity and the generation of reactive oxygen species (ROS), as well as decreased the invasiveness. Treatment of TSGH 9201 cells with erinacine A resulted in the activation of caspases and the expression of TRAIL. Erinacine A induction of apoptosis was accompanied by sustained phosphorylation of FAK/AKT/p70S6K and the PAK1 pathways, as well as the generation of ROS. Furthermore, the induction of apoptosis and anti-invasion properties by erinacine A could involve the differential expression of the 14-3-3 sigma protein (1433S) and microtubule-associated tumor suppressor candidate 2 (MTUS2), with the activation of the FAK/AKT/p70S6K and PAK1 signaling pathways. Conclusions: These results lead us to speculate that erinacine A may generate an apoptotic cascade in TSGH 9201 cells by activating the FAK/AKT/p70S6K/PAK1 pathway and upregulating proteins 1433S and MTUS2, providing a new mechanism underlying the anti-cancer effects of erinacine A in human gastric cancer cells.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000480338
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
    Location Call Number Limitation Availability
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