Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
PLoS One. 2013 Apr 26;8(4):e61379. doi: 10.1371/journal.pone.0061379. Print 2013.
Biomarker discovery using mass spectrometry (MS) has recently seen a significant increase in applications, mainly driven by the rapidly advancing field of metabolomics. Instrumental and data handling advancements have allowed for untargeted metabolite analyses which simultaneously interrogate multiple biochemical pathways to elucidate disease phenotypes and therapeutic mechanisms. Although most MS-based metabolomic approaches are coupled with liquid chromatography, a few recently published studies used matrix-assisted laser desorption (MALDI), allowing for rapid and direct sample analysis with minimal sample preparation. We and others have reported that prostaglandin E3 (PGE3), derived from COX-2 metabolism of the omega-3 fatty acid eicosapentaenoic acid (EPA), inhibited the proliferation of human lung, colon and pancreatic cancer cells. However, how PGE3 metabolism is regulated in cancer cells, particularly human non-small cell lung cancer (NSCLC) cells, is not fully understood. Here, we successfully used MALDI to identify differences in lipid metabolism between two human non-small-cell lung cancer (NSCLC) cell lines, A549 and H596, which could contribute to their differential response to EPA treatment. Analysis by MALDI-MS showed that the level of EPA incorporated into phospholipids in H596 cells was 4-fold higher than A549 cells. Intriguingly, H596 cells produced much less PGE3 than A549 cells even though the expression of COX-2 was similar in these two cell lines. This appears to be due to the relatively lower expression of cytosolic phospholipase A2 (cPLA2) in H596 cells than that of A549 cells. Additionally, the MALDI-MS approach was successfully used on tumor tissue extracts from a K-ras transgenic mouse model of lung cancer to enhance our understanding of the mechanism of action of EPA in the in vivo model. These results highlight the utility of combining a metabolomics workflow with MALDI-MS to identify the biomarkers that may regulate the metabolism of omega-3 fatty acids and ultimately affect their therapeutic potentials.
基于质谱(MS)的生物标志物发现最近在应用中显著增加,主要由代谢组学的快速发展推动。仪器和数据处理的进步使得能够进行非靶向代谢物分析,同时检测多个生化途径以阐明疾病表型和治疗机制。尽管大多数基于 MS 的代谢组学方法与液相色谱法相结合,但最近发表的一些研究使用基质辅助激光解吸(MALDI),允许进行快速和直接的样品分析,样品制备最少。我们和其他人已经报道了前列腺素 E3(PGE3),源自 ω-3 脂肪酸二十碳五烯酸(EPA)的 COX-2 代谢,抑制了人类肺、结肠和胰腺癌细胞的增殖。然而,PGE3 代谢在癌细胞中是如何调节的,特别是在人类非小细胞肺癌(NSCLC)细胞中,尚未完全了解。在这里,我们成功地使用 MALDI 来鉴定两种人类非小细胞肺癌(NSCLC)细胞系 A549 和 H596 之间的脂质代谢差异,这可能有助于它们对 EPA 治疗的不同反应。MALDI-MS 分析表明,H596 细胞中 EPA 掺入磷脂的水平比 A549 细胞高 4 倍。有趣的是,尽管这两种细胞系中 COX-2 的表达相似,但 H596 细胞产生的 PGE3 比 A549 细胞少得多。这似乎是由于 H596 细胞中胞质型磷脂酶 A2(cPLA2)的表达相对低于 A549 细胞。此外,MALDI-MS 方法成功地应用于肺癌 K-ras 转基因小鼠模型的肿瘤组织提取物,以增强我们对 EPA 在体内模型中作用机制的理解。这些结果强调了将代谢组学工作流程与 MALDI-MS 相结合以鉴定可能调节 ω-3 脂肪酸代谢并最终影响其治疗潜力的生物标志物的实用性。