Photodynamic Therapy Resistant Human Colon Carcinoma HT29 Cells Show Cross‐Resistance to UVA but not UVC Light

Photodynamic Therapy Resistant Human Colon Carcinoma HT29 Cells Show Cross‐Resistance to UVA but not UVC Light
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光动力疗法耐药的人结肠癌 HT29 细胞对 UVA 表现出交叉耐药性,但对 UVC 没有交叉耐药性

DOI:
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发表时间:
2007
影响因子:
3.3
通讯作者:
A. Rainbow
A. Rainbow
中科院分区:
生物学3区
文献类型:
--
作者:
Natalie J. Zacal;A. Rainbow

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The isolation of photodynamic therapy (PDT)‐resistant HT29 human colon adenocarcinoma cells has been reported previously. These PDT‐resistant variants show increased expression of the Hsp27 and BNip3 proteins and a decreased expression of mutant p53 protein compared with parental HT29 cells. Because mutant p53 and increased expression of Hsp27 have been associated with resistance to various chemotherapeutic agents, whereas BNip3 is a potent inducer of apoptosis, we were interested in determining whether these PDT‐resistant cells were cross‐resistant to other cytotoxic agents. In the present report, we examined the colony survival of the PDT‐resistant HT29 variants and several other clonal variants of HT29 cells to ultraviolet light (UV) treatment. The HT29 PDT‐resistant variants showed cross‐resistance to long‐wavelength UVA (320–400 nm) but not to short‐wavelength UVC (200–280 nm) light. Cell sensitivity to UVA or UVC was then correlated with Hsp27, BNip3 and mutant p53 protein levels in the PDT‐resistant variants as well as in several clonal variants of HT29 cells that express different levels of Hsp27, BNip3 and mutant p53. We show that increased expression of Hsp27 and BNip3 and decreased expression of mutant p53 correlated with increased resistance to UVA. In contrast, increased expression of Hsp27 and BNip3 correlated with increased sensitivity to UVC, whereas increased expression of mutant p53 showed no significant correlation with sensitivity to UVC. These results suggest that the PDT‐resistant HT29 cell variants are differentially sensitized to UVA compared with UVC due, in part at least, through the altered expression levels of BNip3, Hsp27 and mutant p53.
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