This study is to analyze the potential contribution of Syndecan 1 (SDC1) to cisplatin resistance in hepatic carcinoma. Cell proliferation and viability were determined by direct counting and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, respectively. The protein levels of SDC1, p-AKT, AKT and β-actin were quantified by western blotting. The SDC1 transcript abundance was measured by real-time polymerase chain reaction. The relative expression of SDC1 in clinical liver tumor samples was analyzed with immunohistochemistry. SDC1 was up-regulated in cisplatin-resistant HepG2 cells (denoted as HepG2 CR hereafter). SDC1-knockdown re-sensitized HepG2 CR cells to cisplatin treatment. Ectopic over-expression of SDC1 conferred drug resistance to naïve HepG2 cells. PI3K/AKT pathway was over-activated in HepG2 CR cells, and simultaneous administration with PI3K inhibitor greatly surmounted the resistance. We also demonstrated that SDC1 was aberrantly up-regulated in clinical hepatocellular carcinoma samples. Our study highlighted the importance of SDC1-PI3K/AKT signaling in the cisplatin resistance in hepatocellular carcinoma.

中文翻译：

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SDC1通过PI3K-AKT途径促进肝癌细胞的顺铂耐药性。

本研究旨在分析Syndecan 1（SDC1）对肝癌顺铂耐药性的潜在作用。细胞增殖和活力分别通过直接计数和3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物测定来确定。通过蛋白质印迹定量SDC1，p-AKT，AKT和β-肌动蛋白的蛋白质水平。通过实时聚合酶链反应测量SDC1转录丰度。用免疫组织化学分析SDC1在临床肝肿瘤样品中的相对表达。SDC1在顺铂耐药的HepG2细胞（以下称为HepG2 CR）中上调。SDC1组合式使HepG2 CR细胞重新敏化为顺铂治疗。SDC1的异位过表达赋予了对纯天然HepG2细胞的耐药性。在HepG2 CR细胞中，PI3K / AKT通路被过度激活，同时使用PI3K抑制剂可大大克服耐药性。我们还证明在临床肝细胞癌样本中SDC1异常上调。我们的研究强调了SDC1-PI3K / AKT信号在肝细胞癌顺铂耐药中的重要性。