Özet:

Abstract Multidrug Resistance is a major obstacle in cancer chemotherapy. The current study was designed to evaluate the multidrug resistance and apoptotic properties of Hepatoma cells. Antiproliferative effect of five anti-cancer drugs: three of bacterial origin namely, puromycin, actinomycin D, doxorubicin and two plant derived drugs viz., colchicine and vinblastine were assessed on heat- resistant variants of dexamethasone–resistant and the dexamethasone- sensitive variants of hepatoma cell lines. These variants showed increased drug resistance to the different anticancer drugs used, i.e., they became moderately multidrug-resistant. The severely heat-treated H56 cells became moderately resistant only to certain drugs. All the experimental variants of Hepatoma cells overexpressed functional P-glycoprotein, a drug-resistant associated marker protein, which attributes to the resistance shown by these cells. The anticancer drugs were capable of inducing apoptosis in both H56 and clone 2 cells and it was found that H56 cells were more prone to undergo apoptosis as compared to clone 2 cells. Furthermore, preliminary immunocytochemical studies revealed that there was a significant difference in expression of p53, a tumor suppressor gene, in H56 and clone 2 cells where H56 cells showed very strong staining for p53 thereby justifying their proneness to apoptosis.

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