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首页> 外文期刊>American Journal of Physiology >Parathyroid hormone-related protein ameliorates death receptor-mediated apoptosis in lung cancer cells.
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Parathyroid hormone-related protein ameliorates death receptor-mediated apoptosis in lung cancer cells.

机译：甲状旁腺激素相关蛋白可改善肺癌细胞中死亡受体介导的凋亡。

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摘要

Parathyroid hormone-related protein (PTHrP) is expressed in more advanced, aggressive tumors and may play an active role in cancer progression. This study investigated the effects of PTHrP on apoptosis after UV irradiation, Fas ligation, or staurosporine treatment in BEN human squamous lung carcinoma cells. Cells at 70% confluency were treated for 24 h with 100 nM PTHrP-(1-34), PTHrP-(38-64), PTHrP-(67-86), PTHrP-(107-139), or PTHrP-(140-173) in media with serum, exposed for 30 min to UV-B radiation (0.9 mJ/cm2), and maintained for another 24 h. Caspase-3, caspase-8, and caspase-9 activities increased fivefold. Pretreatment with PTHrP-(1-34) and PTHrP-(140-173) ameliorated apoptosis after UV irradiation, as indicated by reduced caspase activities, increased cell protein, decreased nuclear condensation, and increased clonal survival. Other peptides had no effect on measures of apoptosis. PTHrP-(140-173) also reduced caspase activities after Fas ligation by activating antibody, but neither peptide had effects on caspase-3 or caspase-9 activity after 1 microM staurosporine. These data indicate that PTHrP-(1-34) and PTHrP-(140-173) protect against death receptor-induced apoptosis in BEN lung cancer cells but are ineffective against mitochondrial pathways. PTHrP contributes to lung cancer cell survival in culture and could promote cancer progression in vivo. The mechanism for the protective effect against apoptosis remains to be determined.
机译：甲状旁腺激素相关蛋白（PTHrP）在较晚期的侵袭性肿瘤中表达，并可能在癌症进展中发挥积极作用。这项研究调查了PTHrP对BEN人鳞状上皮癌细胞UV照射，Fas连接或星形孢菌素处理后凋亡的影响。用100 nM PTHrP-（1-34），PTHrP-（38-64），PTHrP-（67-86），PTHrP-（107-139）或PTHrP-（140）处理70％汇合的细胞24小时-173）在含血清的培养基中，暴露于UV-B辐射（0.9 mJ / cm2）30分钟，并再保持24小时。 Caspase-3，caspase-8和caspase-9活性增加了五倍。 PTHrP-（1-34）和PTHrP-（140-173）预处理可改善紫外线照射后的细胞凋亡，如胱天蛋白酶活性降低，细胞蛋白增加，核浓缩减少和克隆存活率提高所表明的。其他肽对细胞凋亡的测量没有影响。 PTHrP-（140-173）也可以通过激活抗体降低Fas连接后的caspase活性，但是1 microM星形孢菌素后，两种肽都不会对caspase-3或caspase-9活性产生影响。这些数据表明PTHrP-（1-34）和PTHrP-（140-173）可以保护BEN肺癌细胞免受死亡受体诱导的凋亡，但对线粒体途径无效。 PTHrP有助于培养中的肺癌细胞存活，并可能促进体内癌症的发展。抗凋亡保护作用的机制尚待确定。

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