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首页> 外文会议>Optical methods for tumor treatment and detection: Mechanisms and techniques in photodynamic therapy XVIII >Autophagy in response to photodynamic therapy: Cell survival vs. cell death
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Autophagy in response to photodynamic therapy: Cell survival vs. cell death

机译：对光动力疗法的自噬：细胞存活与细胞死亡

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Autophagy (or more properly, macroautophagy) is a pathway whereby damaged organelles or other cell components are encased in a double membrane, the autophagosome, which fuses with lysosomes for digestion by lysosomal hydrolases. This process can promote cell survival by removing damaged organelles, but when damage is extensive, it can also be a mechanism of cell death. Similar to the Kessel and Agostinis laboratories, we have reported the vigorous induction of autophagy by PDT; this was found in human breast cancer MCF-7 cells whether or not they were able to efficiently induce apoptosis. One way to evaluate the role of autophagy in PDT-treated cells is to silence one of the essential genes in the pathway. Kessel and Reiners silenced the Atg7 gene of murine leukemia LI210 cells using inhibitory RNA and found sensitization to PDT-induced cell death at a low dose of PDT, implying that autophagy is protective when PDT damage is modest. We have examined the role of autophagy in an epithelium-derived cancer cell by comparing parental and Atg7-silenced MCF-7 cells to varying doses of PDT with the phthalocyanine photosensitizer Pc 4. In contrast to L1210 cells, autophagy-deficient MCF-7 cells were more resistant to the lethal effects of PDT, as judged by clonogenic assays. A possible explanation for the difference in outcome for L1210 vs. MCF-7 cells is the greatly reduced ability of the latter to undergo apoptosis, a deficiency that may convert autophagy into a cell-death process even at low PDT doses. Experiments to investigate the mechanism(s) responsible are in process.
机译：自噬（或更恰当的说，是自噬）是一种途径，通过这种途径，受损的细胞器或其他细胞成分被包裹在双层膜中，即自噬体，与溶酶体融合，通过溶酶体水解酶进行消化。该过程可以通过去除受损的细胞器来促进细胞存活，但是当损伤广泛时，它也可能是细胞死亡的机制。与Kessel和Agostinis实验室相似，我们已经报道了PDT对自噬的强烈诱导。在人类乳腺癌MCF-7细胞中发现了这一点，无论它们是否能够有效诱导凋亡。评估自噬在PDT处理的细胞中的作用的一种方法是沉默该途径中的必需基因之一。 Kessel和Reiners使用抑制性RNA沉默了鼠白血病LI210细胞的Atg7基因，发现在低剂量的PDT下对PDT诱导的细胞死亡敏感，这意味着当PDT损伤适度时自噬是保护性的。我们已经通过将亲本和Atg7沉默的MCF-7细胞与不同剂量的PDT 4和酞菁光敏剂Pd进行比较，研究了自噬在上皮来源的癌细胞中的作用。与L1210细胞相比，自噬缺陷型MCF-7细胞克隆形成试验表明，它们对PDT的致死作用更具抵抗力。 L1210与MCF-7细胞结局差异的可能解释是后者的凋亡能力大大降低，即使在低PDT剂量下，这种缺陷也可能将自噬转变为细胞死亡过程。正在调查负责机制的实验。

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