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Article: Pharmacological inhibition of protein kinase C activity could induce apoptosis in gastric cancer cells by differential regulation of apoptosis- related genes

TitlePharmacological inhibition of protein kinase C activity could induce apoptosis in gastric cancer cells by differential regulation of apoptosis- related genes
Authors
KeywordsApoptosis
bcl-2
c-myc
Cell cycle
Gastric cancer
p53
Protein kinase C
Issue Date1999
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116
Citation
Digestive Diseases And Sciences, 1999, v. 44 n. 10, p. 2020-2026 How to Cite?
AbstractThe protein kinase C (PKC) signaling pathway plays a key role in tumor cell proliferation, differentiation, and apoptosis. Gastric cancer usually possesses a higher level of PKC activity than normal tissue. We evaluated inhibition of PKC activity in apoptosis induction of gastric cancer cells and the expression profile of apoptosis-related genes. Gastric cancer cells (AGS) were incubated with two highly specific PKC inhibitors (RO-31-8220 and chelerythrine). Cell viability and cell cycle were determined by methyl- tetrazolium (MTT) assay and flow cytometry, respectively. Apoptosis was characterized by acridine orange staining, DNA gel electrophoresis, and flow cytometry. The expression of p53, p21(waf/cip1), c-myc, bcl-2, and bax was determined by western blot. The results showed that both PKC inhibitors hindered cell growth, arrested cells at G0/G1 phase and induced apoptosis. The protein level of p53, p21(waf/cip1), c-myc, and bax was elevated while bcl-2 kept unchanged following drug exposure. In conclusion, PKC inhibitors suppress growth of gastric cancer cells through apoptosis induction and cell cycle quiescence, which may be regulated by differential expression of apoptosis-related genes.
Persistent Identifierhttp://hdl.handle.net/10722/162278
ISSN
2021 Impact Factor: 3.487
2020 SCImago Journal Rankings: 1.140
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhu, GHen_US
dc.contributor.authorWong, BCYen_US
dc.contributor.authorEggo, MCen_US
dc.contributor.authorYuen, STen_US
dc.contributor.authorLai, KCen_US
dc.contributor.authorLam, SKen_US
dc.date.accessioned2012-09-05T05:18:36Z-
dc.date.available2012-09-05T05:18:36Z-
dc.date.issued1999en_US
dc.identifier.citationDigestive Diseases And Sciences, 1999, v. 44 n. 10, p. 2020-2026en_US
dc.identifier.issn0163-2116en_US
dc.identifier.urihttp://hdl.handle.net/10722/162278-
dc.description.abstractThe protein kinase C (PKC) signaling pathway plays a key role in tumor cell proliferation, differentiation, and apoptosis. Gastric cancer usually possesses a higher level of PKC activity than normal tissue. We evaluated inhibition of PKC activity in apoptosis induction of gastric cancer cells and the expression profile of apoptosis-related genes. Gastric cancer cells (AGS) were incubated with two highly specific PKC inhibitors (RO-31-8220 and chelerythrine). Cell viability and cell cycle were determined by methyl- tetrazolium (MTT) assay and flow cytometry, respectively. Apoptosis was characterized by acridine orange staining, DNA gel electrophoresis, and flow cytometry. The expression of p53, p21(waf/cip1), c-myc, bcl-2, and bax was determined by western blot. The results showed that both PKC inhibitors hindered cell growth, arrested cells at G0/G1 phase and induced apoptosis. The protein level of p53, p21(waf/cip1), c-myc, and bax was elevated while bcl-2 kept unchanged following drug exposure. In conclusion, PKC inhibitors suppress growth of gastric cancer cells through apoptosis induction and cell cycle quiescence, which may be regulated by differential expression of apoptosis-related genes.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116en_US
dc.relation.ispartofDigestive Diseases and Sciencesen_US
dc.subjectApoptosis-
dc.subjectbcl-2-
dc.subjectc-myc-
dc.subjectCell cycle-
dc.subjectGastric cancer-
dc.subjectp53-
dc.subjectProtein kinase C-
dc.subject.meshAdenocarcinoma - Pathologyen_US
dc.subject.meshAlkaloidsen_US
dc.subject.meshApoptosis - Geneticsen_US
dc.subject.meshBenzophenanthridinesen_US
dc.subject.meshCell Cycle - Drug Effectsen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshPhenanthridines - Pharmacologyen_US
dc.subject.meshProtein Kinase C - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshStomach Neoplasms - Pathologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titlePharmacological inhibition of protein kinase C activity could induce apoptosis in gastric cancer cells by differential regulation of apoptosis- related genesen_US
dc.typeArticleen_US
dc.identifier.emailWong, BCY:bcywong@hku.hken_US
dc.identifier.authorityWong, BCY=rp00429en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1023/A:1026670301787en_US
dc.identifier.pmid10548353-
dc.identifier.scopuseid_2-s2.0-0032712229en_US
dc.identifier.hkuros50515-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032712229&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume44en_US
dc.identifier.issue10en_US
dc.identifier.spage2020en_US
dc.identifier.epage2026en_US
dc.identifier.isiWOS:000083352500015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhu, GH=7402633170en_US
dc.identifier.scopusauthoridWong, BCY=7402023340en_US
dc.identifier.scopusauthoridEggo, MC=7006000548en_US
dc.identifier.scopusauthoridYuen, ST=7103160927en_US
dc.identifier.scopusauthoridLai, KC=7402135595en_US
dc.identifier.scopusauthoridLam, SK=7402279473en_US
dc.identifier.issnl0163-2116-

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