2016年12月
光線力学的処置によるPaclitaxel耐性獲得HeLa細胞の耐性低減
生体医工学
- 巻
- 54
- 号
- 6
- 開始ページ
- 245
- 終了ページ
- 252
- 記述言語
- 日本語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.11239/jsmbe.54.245
- 出版者・発行元
- 一般社団法人 日本生体医工学会
<p>Photodynamic therapy (PDT) is used for the treatment of malignant tumors. It is based on the interaction of a photosensitizer with light of appropriate wavelength in the presence of molecular oxygen. In recent years, applications of PDT have been extended to conditions other than superficial, early-stage cancers. The therapy leads to inhibition of angiogenesis, and hence has been applied also to the treatment of age-related macular degeneration. Recently, PDT has been reported to potentially reduce cell membrane permeability. In this study, we evaluated the efficacy of PDT, focusing on its ability to regulate cell or tissue functions. In particular, we studied the potential of PDT to reduce acquired resistance to anticancer agents in cell types over-expressing P-glycoprotein (P-gp), a membrane-bound drug efflux transporter. Photofrin®(PF) was used as the photosensitizing agent. Irradiation was performed in the range of 0.5-3.0 J/cm2, which did not lead to any significant cytotoxic effect. The contact between PF and target cells was facilitated by adding PF in (1)a serum-containing culture medium (Protocol 1), and (2)phosphate-buffered saline (Protocol 2). HeLa cells were incubated in these two culture media. A comparative assessment was employed to evaluate the capacity of PDT to reduce acquired resistance to paclitaxel (TXL) in these cells. Although there was no significant reduction in TXL resistance by PDT in Protocol 1, a decrease in drug efflux activity was obtained in Protocol 2, indicating a reduction in TXL resistance. The results of this study suggest that administration of PDT under specific conditions leads to reduction in drug efflux capacity of cells with acquired resistance to anticancer agents.</p>
- リンク情報
- ID情報
-
- DOI : 10.11239/jsmbe.54.245
- ISSN : 1347-443X
- CiNii Articles ID : 130005450574
- CiNii Books ID : AA11633569