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首页> 外文会议>Optical methods for tumor treatment and detection: mechanisms and techniques in photodynamic therapy XX >Combination of PI3K/Akt/mTOR inhibitors and PDT in endothelial and tumor cells.
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Combination of PI3K/Akt/mTOR inhibitors and PDT in endothelial and tumor cells.

机译：内皮细胞和肿瘤细胞中PI3K / Akt / mTOR抑制剂和PDT的组合。

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摘要

The PI3/Akt/mTOR kinase signaling pathway is a major signaling pathway in eukaryotic cells, and dysregulation of this signaling pathway has been implicated in tumorigenesis and malignancy in several cancers including prostate cancer. We assessed the effects of combination PI3K pathway inhibition on the efficacy of PDT in human prostate tumor cell line (PC3) and SV40-transformed mouse endothelial cell line (SVEC-40). Combination of PDT and BEZ 235 (BEZ), a pan-PI3/ mTOR kinase inhibitor additively enhanced efficacy of sub-lethal PDT in both cell lines. The combination of the pan-PI3/ mTOR kinase inhibitor LY294002 (LY) with PDT also enhanced efficacy of PDT in PC3 in an additive manner but synergistically in SVEC. In order to determine the mechanism of enhancement of efficacy, we assessed apoptosis and autophagy following PDT. PDT-mediated apoptosis was enhanced in endothelial cells, by both BEZ and LY rapidly after treatment. Compared to SVEC, PC3 cells are apoptosis-deficient and apoptosis was not significantly enhanced by either LY or BEZ. However, lethal PDT of PC3 cells induced a delayed autophagic response which may be enhanced by combination, depending on PI3K inhibitor and dose.
机译：PI3 / Akt / mTOR激酶信号传导途径是真核细胞中的主要信号传导途径，并且该信号传导途径的失调与包括前列腺癌在内的多种癌症的肿瘤发生和恶性肿瘤有关。我们评估了组合PI3K途径抑制对人前列腺肿瘤细胞系（PC3）和SV40转化的小鼠内皮细胞系（SVEC-40）中PDT功效的影响。 PDT和pan-PI3 / mTOR激酶抑制剂BEZ 235（BEZ）的组合可在两种细胞系中共同增强亚致死性PDT的功效。 pan-PI3 / mTOR激酶抑制剂LY294002（LY）与PDT的组合也以相加的方式增强了PC3中PDT的功效，但在SVEC中具有协同作用。为了确定功效增强的机制，我们评估了PDT后的凋亡和自噬。在治疗后，BEZ和LY均可迅速促进PDT介导的内皮细胞凋亡。与SVEC相比，PC3细胞凋亡不足，而LY或BEZ均未显着增强细胞凋亡。但是，PC3细胞的致死性PDT诱导了延迟的自噬反应，这可能通过结合来增强，具体取决于PI3K抑制剂和剂量。

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