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To investigate acquired paclitaxel (PTX) resistance in cancer cells, weestablished five monoclonal PTX-resistant cell lines from HEC-1 human endometrialadenocarcinoma cells by means of long-term PTX-exposed cultures and limiting dilutioncultures. The established PTX-resistant subclones showed apparent resistance toPTX-induced DNA fragmentation but not to PTX-induced growth suppression. Noneof the five PTX-resistant subclones showed apparent resistance to other anticancerdrugs such as cisplatin, etoposide, 5-fluorouracil, pirarubicin-HCl, 4-hydroxy-cyclophosphamideor mitomycin C. Semiquantitative flow cytometric analysis revealed no apparentdifferential expression of 17 molecules that were previously reported to regulateapoptosis or drug resistance, between the five PTX-resistant subclones and theparent cells. Karyotyping analysis revealed common changes in chromosomes 4 and18 in the five PTX-resistant subclones but not in the HEC-1 parent cells. Theseresults indicate that PTX-induced growth suppression is regulated by differentmechanisms from those involved in PTX-induced apoptosis. It was concluded thatthese established PTX-resistant subclones can be useful models in studies relatedto the prevention or treatment of recurrent cancers after PTX chemotherapy.

international journal of oncology

Differential sensitivity to paclitaxel-induced apoptosis and growth suppression in paclitaxel-resistant cell lines established from HEC-1 human endometrial adenocarcinoma cells