Dissertation
Dissertation > Medicine, health > Oncology > Gastrointestinal Cancer > Gastric neoplasms

Effects of Proliferation and Apoptosis of Gastric Carcinoma Cell Line Sgc-7901 by Cetuximab (Erbitux)

Author LuoSuQing
Tutor GuanHongGeng
School Suzhou University
Course Department of General Surgery
Keywords gastric carcinoma cell SGC-7901 Cetuximab apoptosis bcl-2 caspase-3 P-27
CLC R735.2
Type Master's thesis
Year 2011
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Objective:To investigate the anti-tumor effect and its mechanisms of Cetuximab on human gastric carcinoma cell line SGC-7901 in vitro.Methods:In vitro,human gastric carcinoma cell line SGC-7901 was treated by Cetuximab in different concentrations.The inhibitory effect of cell growth was assayed by MTT assay;cell cycles and apoptosis were analyzed by flow cytometry (FCM);the mRNA expressions of bcl-2, caspase-3,P-27 were analyzed by RT-PCR; Immunohistochemistry was used to detect bcl-2,caspase-3,P-27 protein expression.Results: (1)MTT assay indicated that the inhibitory effect of Cetuximab on the proliferation of SGC-7901 cell was found in dose– and–time dependent manner. There was great statistical signification between varies medicated group and control group(P<0.05),and there also were great statistical signification between medicated group each other (P<0.05) . (2) Comparing with control group,the cell apoptosis was induced by Cetuximab at 48 hours,meanwhile,the ratio of G0/G1 phase was increased and the ratio of S phase was decreased, in dose-dependent manner(P<0.05). (3)RT-PCR assay and Immunocytochemistry showed that the expression of caspase-3,P-27 mRNA and protein were upregulated and bcl-2 mRNA and protein was downregulated by Cetuximab at 48 hours with concentration increased(P<0.05).Conclusion:The growth of SGC-7901 cell in vitro is inhibited by Cetuximab and in dose-and-time dependent manner. Cetuximab also can arrest cell cycle at G0/G1phase,induce cell apoptosis.Maybe its mechanism is through upregulating the expressions of caspase-3,P-27 mRNA and protein,downreglating the espression of bcl-2mRNA and protein.

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