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  • 1
    Electronic Resource
    Electronic Resource
    Pharmacological Inhibition of Protein Kinase C Activity Could Induce Apoptosis in Gastric Cancer Cells by Differential Regulation of Apoptosis-Related Genes (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 2020-2026 
    Details
    ISSN: 1573-2568
    Keywords: APOPTOSIS ; PROTEIN KINASE C ; CELL CYCLE ; GASTRIC CANCER
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The protein kinase C (PKC) signaling pathwayplays a key role in tumor cell proliferation,differentiation, and apoptosis. Gastric cancer usuallypossesses a higher level of PKC activity than normaltissue. We evaluated inhibition of PKC activity inapoptosis induction of gastric cancer cells and theexpression profile of apoptosis-related genes. Gastriccancer cells (AGS) were incubated with two highlyspecific PKC inhibitors (RO-31-8220 and chelerythrine).Cell viability and cell cycle were determined bymethyl-tetrazolium (MTT) assay and flow cytometry,respectively. Apoptosis was characterized by acridineorange staining, DNA gel electrophoresis, and flowcytometry. The expression of p53,p21waf/cip1, c-myc, bcl-2, and bax wasdetermined by western blot. The results showed that bothPKC inhibitors hindered cell growth, arrested cells atG0/G1 phase and induced apoptosis.The protein level of p53, p21waf/cip1, c-myc,and bax was elevated while bcl-2 kept unchangedfollowing drug exposure. In conclusion, PKC inhibitorssuppress growth of gastric cancer cells throughapoptosis induction and cell cycle quiescence, which maybe regulated by differential expression ofapoptosis-related genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026670301787
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  • 2
    Electronic Resource
    Electronic Resource
    Nonsteroidal Antiinflammatory Drugs Could Reverse Helicobacter pylori-Induced Apoptosis and Proliferation in Gastric Epithelial Cells (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 1957-1963 
    Details
    ISSN: 1573-2568
    Keywords: APOPTOSIS ; PROLIFERATION ; HELICOBACTER PYLORI ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; STOMACH
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It remains controversial whether the harmfuleffects of Helicobacter pylori (Hp) and nonsteroidalantiinflammatory drugs (NSAIDs) are additive. We studiedthe effects of Hp (virulent and nonvirulent strains) and NSAIDs, alone or in combination, onapoptosis and proliferation of gastric epithelial cellsin nonulcer dyspepsia (NUD) patients. Forty-four (25Hppositive and 19 Hp-negative) consecutive Chinese NUD patients with rheumatoid arthritis who hadtaken continuously NSAIDs for more than three monthswere recruited for this study. Another 41 (20Hp-positive and 21 Hp-negative) NUD patients not on anyNSAIDs were included as controls. All patientsunderwent a gastroscopy examination and gastricbiopsies. Hp infection was confirmed by CLOtest, anti-HpELISA, and [13C]urea breath test. The CagAstatus was determined by the anti-CagA antibody assay. The degree ofgastritis, apoptosis, and proliferation indices weredetermined with H&E staining, terminal uridinedeoxynucleotidyl nick end-labeling (TUNEL), andproliferating cell nuclear antigen (PCNA) immunostainingmethods, respectively. A significantly higher apoptosiswas observed in subjects who had Hp infection or hadbeen consuming NSAIDs when compared with the controls. Unlike NSAID-treated subjects, patients with Hpinfection were shown to have significantly enhanced cellproliferation. However, the increased apoptosis andproliferation in Hp-positive subjects were reversed by also taking NSAIDs. No correlation was foundbetween apoptosis and proliferation in all the studygroups. There was no association found between CagAexpression or degree of gastritis with cellproliferation or apoptosis. It was demonstrated at thecellular level that NSAIDs could abrogate apoptosis orproliferation effects induced by Hp. Furthermore, thelatter effects appeared not to be influenced by the virulent nature of the Hp strains.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018830408397
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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