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

Tanaka,Tetsuji; Toujima,Saori; Tanaka,Junko

doi:10.3892/ijo.2012.1600

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

Authors:
- Tetsuji Tanaka
- Saori Toujima
- Junko Tanaka
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Affiliations: Santamaria Hospital, Ibaraki, Osaka 567-0884, Japan, Department of Obstetrics and Gynecology, Wakayama Medical University, Wakayama 641-0012, Japan, Graduate School of Intercultural Studies, Kobe University, Nada-ku, Kobe 657-8501, Japan
Published online on: August 22, 2012 https://doi.org/10.3892/ijo.2012.1600
Pages: 1837-1844

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Abstract

To investigate acquired paclitaxel (PTX) resistance in cancer cells, we established five monoclonal PTX-resistant cell lines from HEC-1 human endometrial adenocarcinoma cells by means of long-term PTX-exposed cultures and limiting dilution cultures. The established PTX-resistant subclones showed apparent resistance to PTX-induced DNA fragmentation but not to PTX-induced growth suppression. None of the five PTX-resistant subclones showed apparent resistance to other anticancer drugs such as cisplatin, etoposide, 5-fluorouracil, pirarubicin-HCl, 4-hydroxy-cyclophosphamide or mitomycin C. Semiquantitative flow cytometric analysis revealed no apparent differential expression of 17 molecules that were previously reported to regulate apoptosis or drug resistance, between the five PTX-resistant subclones and the parent cells. Karyotyping analysis revealed common changes in chromosomes 4 and 18 in the five PTX-resistant subclones but not in the HEC-1 parent cells. These results indicate that PTX-induced growth suppression is regulated by different mechanisms from those involved in PTX-induced apoptosis. It was concluded that these established PTX-resistant subclones can be useful models in studies related to the prevention or treatment of recurrent cancers after PTX chemotherapy.

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