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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adenoviridae, Antineoplastic Agents, Blotting, Western, Caspase 3, Caspases, Cell Division, Cell Line, Tumor, Cell Survival, Cisplatin, Dose-Response Relationship, Drug, Enzyme Activation, Humans, Protein Kinase C, Protein Kinase C-delta, Recombinant Fusion Proteins, Stomach Neoplasms, Transfection, Tumor Suppressor Protein p53.
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Does overexpression of protein kinase Cdelta enhance cisplatin-induced cytotoxicity correlated with p53 in gastric cancer cell line? Context: An important issue in cancer therapy is to investigate the mechanism for cellular sensitivity to anticancer agents such as cisplatin. Cisplatin is one of the DNA-damaging agents and several factors including p53 are related to the sensitivity to cisplatin in cancer. Protein kinase C (PKC) delta is known as a positive regulator for cisplatin-induced cell death. In our present study, we examined whether overexpression of PKCdelta and p53 increases the sensitivity of the human gastric cancer cell line, MKN28, which has a mutation of p53 gene, to cisplatin. Cell viability and DNA content were measured in MKN28 with adenovirus-mediated expression of PKCdelta and p53 after exposure to cisplatin. In addition, the active form of caspase-3 was detected by Western blotting. Overexpression of exogenous PKCdelta did not induce cell death in MKN28 but inhibited cell growth at 1 microg/ml cisplatin as compared to that by cisplatin alone. Moreover, overexpression of both wild-type p53 and exogenous PKCdelta in MKN28 increased cisplatin-induced cell death in MKN28.
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These results suggest that PKCdelta, in cooperation with p53, possibly regulates cisplatin-induced caspase-3-mediated cell death in gastric cancer. Final Decision: yes