继发性淋巴水肿是妇科恶性肿瘤和乳腺癌淋巴结清扫术后常见的并发症之一。在这项研究中,通过转录组学和代谢组学分析,在分子水平上探讨了PLA2与癌症术后淋巴水肿之间的关系.转录组测序技术,以及代谢组学测定，用于探讨PLA2在淋巴水肿患者中的表达，寻找淋巴水肿发病机制和加重机制的潜在途径。通过培养人淋巴内皮细胞研究sPLA2对人淋巴内皮细胞的作用。分泌型磷脂酶A2(sPLA2)在淋巴水肿组织中呈高表达,然而,细胞质磷脂酶A2（cPLA2），在淋巴水肿中显示低表达，如RT-qPCR所示。通过培养人淋巴管内皮细胞，研究发现，sPLA2引起HLEC空泡化，对HLEC增殖和迁移有抑制作用。通过检测淋巴水肿患者血清中的sPLA2并分析临床资料,发现sPLA2与淋巴水肿的严重程度呈正相关。分泌型磷脂酶A2（sPLA2）在淋巴水肿组织中高表达，损伤淋巴管内皮细胞，与疾病严重程度密切相关，并可作为疾病严重程度的潜在预测因子。缩写:PLA2:磷脂酶A2;DEGs:差异表达基因;DMP:差异代谢产生。
Secondary lymphoedema is one of the common complications after lymph node dissection for gynecologic malignancies and breast cancer. In this study, the relationship between PLA2 and postoperative lymphoedema in cancer at the molecular level has been explored through transcriptomics and metabolomic assays. Transcriptome sequencing technology, as well as metabolomic assays, were utilized to explore the expression of PLA2 in lymphoedema patients, and search for potential pathways in the pathogenesis and exacerbation mechanism of lymphoedema. The effect of sPLA2 on human lymphatic endothelial cells was investigated by culturing human lymphatic endothelial cells. Secretory phospholipases A2 (sPLA2) showed high expression levels in lymphoedema tissues, however, cytoplasmic phospholipases A2 (cPLA2), showed low expression in lymphoedema, as demonstrated by RT-qPCR. By culturing human lymphatic vascular endothelial cells, the study found that sPLA2 causes HLEC vacuolization and has an inhibitory effect on HLEC proliferation and migration. By detecting sPLA2 in the serum of lymphoedema patients and analyzing clinical data, it was found that sPLA2 was positively correlated with the severity of lymphoedema. Secretory Phospholipase A2 (sPLA2) is highly expressed in lymphoedema tissue, damages lymphatic vessel endothelial cells, is strongly associated with disease severity, and can be used as a potential predictor of disease severity.Abbreviations: PLA2: Phospholipase A2; DEGs: differentially expressed genes; DMP: differential metabolic production.
