Cancer chemotherapy with taxol often fails due to acquired resistance of cancer cells, which is frequently associated with an overexpression of P-gp and alterations of beta -tubulin. A taxol-resistant cell line, QGY-TR50, derived from a human hepatocellular carcinoma (HCC) QGY-7703 cell line was used to investigate the mechanisms of taxol-resistance, QGY-TR50 cells showed more than 250-fold resistance to taxol and exhibited cross-resistance to other drugs including actinomycin D, doxorubicin, vinblastine, and vincristine, P-gp was highly expressed in QGY-TR50 cells. Expression levels of five human beta -tubulin isotypes (beta (I), beta (II)-, beta (III)-, beta (IVa), and beta (IVb)-tubulin) were examined by real-time semi-quantitative PCR. Comparing with QGY-7703 cells, QGY-TR50 cells did not show any significant change in the expression levels of beta (I)-, beta (IVa), and beta (IVb)-tubulin, While a 1.2-fold increased in beta (II)-tubulin and a 0.5-fold decreased in beta (III)-tubulin levels were observed. All results suggest that the P-glycoprotein could be one key factor involved in enhancing drug resistance in QGY-TR50 cells.