| Purpose: To explore whether and how Cetuximab, an anti-EGFR monoclonalantibody, could enhance radiosensitivity of human gastric cancer SGC7901cells.Methods: MTT assay was used to determine the effect of Cetuximab onSGC7901cell growth inhibition. SGC7901cells was treated with or withoutCetuximab and exposed to radiation. Clonogenic survival assay was performed toindentify the radiosensitivity of both groups. SGC7901cells was treated without orwith Cetuximab for48h or72h respectively and exposed to Radiation. Cell apoptosisand cell cycle distribution and progression were assessed with flow cytometry.Results: Cetuximab could not inhibit the proliferation of SCG7901cells inconcentration of25-250ug/ml, and the50%inhibition concentrations(IC50) ofCetuximab in SGC7901cells was1000ug/ml. In clonogenic cell survival assay, thecell survival fraction(SF) was significnatly decreased with the evaluation of radiationdose. When treated with Cetuximab, the radiosensitization enhancement ratio(SER)of SGC7901cells was1.07. In this study, Cetuximab exposure along could notenhance the induction of cell apoptosi（sP>0.05）. However, combined treatment withradiation and Cetuximab(200ug/ml) for72hours resulted in a significant increase inapoptosis of SGC7901cell(P<0.05). Radiation with or without Cetuximab induceaccumulation of SGC7901cells in G2-M phase,while a reduction of cells in G0-G1phase. In this study, Cetuximab exposure alone had no influence on cell cycledistrbution(P>0.05), but when combined with radiation, Cetuximab inducesaccumlation of SGC7901cells in S phase(P<0.05).Conclusion: Cetuximab followed by radiation could mildly increase theradiosensitivity of SGC7901cells. |
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