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Transcriptomic analysis of the effect of ifosfamide on MDCK cells cultivated in microfluidic biochips

机译：异环磷酰胺对微流生物芯片中培养的MDCK细胞影响的转录组学分析

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摘要

We investigated the behavior of renal cells cultivated in microfluidic biochips when exposed to 50 μM of ifosfamide, an antineoplastic drug treatment. The microarray analysis revealed that ifosfamide had any effect in Petri conditions. The microfluidic biochips induced an early inflammatory response in the MDCK in the untreated cells. This was attributed to cells adapting to the dynamics and micro environment created by the biochips. This led to modulations in the mitochondria dysfunction pathway, the Nrf-2 and oxidative stress pathways and some related cancer genes. When exposed to 50 μM of ifosfamide, we detected a modulation of the pathways related to the cancer and inflammation in the MDCK cultivated in the biochips via modulation of the ATM, p53, MAP Kinase, Nrf-2 and NFKB signaling. In addition, the genes identified and related proteins affected by the ifosfamide treatment in the biochips such as TXNRD1, HSP40 (DNAJB4 and DNAJB9), HSP70 (HSPA9), p21 (CDKN1A), TP53, IKBalpha (NFKBIA) are reported to be the molecular targets in cancer therapy. We also found that the integrin pathway was perturbed with the ifosfamide treatment. Finally, the MYC proto-oncogene appeared to be a potential bridge between the integrin signaling and the anti-inflammatory response.
机译：我们研究了暴露于50μM异环磷酰胺（抗肿瘤药治疗）的微流控生物芯片中培养的肾细胞的行为。芯片分析表明异环磷酰胺在陪替氏条件下有任何作用。微流体生物芯片在未处理的细胞中在MDCK中诱导了早期的炎症反应。这归因于细胞适应由生物芯片产生的动力学和微环境。这导致了线粒体功能障碍途径，Nrf-2和氧化应激途径以及一些相关癌症基因的调节。当暴露于50μM的异环磷酰胺中时，我们通过调节ATM，p53，MAP激酶，Nrf-2和NFKB信号转导，检测到了与生物芯片中培养的MDCK中与癌症和炎症相关的途径的调节。此外，据报道，在生物芯片中受异环磷酰胺处理的已鉴定基因和相关蛋白质如TXNRD1，HSP40（DNAJB4和DNAJB9），HSP70（HSPA9），p21（CDKN1A），TP53，IKBalpha（NFKBIA）是分子癌症治疗的目标。我们还发现整合素途径受到异环磷酰胺治疗的干扰。最后，MYC原癌基因似乎是整联蛋白信号传导和抗炎反应之间的潜在桥梁。

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