【佳学基因检测】外泌体基因检测 lncRNA PCAT1 揭示miR-329-3p/Netrin-1-CD146 复合物是肿瘤循环细胞介导的结直肠癌肝转移的药物治疗靶点

品牌基因检测价格表2022年合理性

学习肿瘤基因组学个性化药物选择知悉《J Immunol Res》在. 2022 Aug 31;2022:9916228.发表了一篇题目为《外泌体基因检测 lncRNA PCAT1 揭示miR-329-3p/Netrin-1-CD146 复合物是肿瘤循环细胞介导的结直肠癌肝转移的药物治疗靶点》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Xingbao Fang, Yongping Xu, Kezhi Li, Peiwan Liu, Hong Zhang, Yang Jiang, Jianwei Tang, Yuehong Li 等完成。促进了肿瘤的精准治疗与个性化用药的发展，进一步强调了基因信息检测与分析的重要性。

肿瘤靶向药物及精准治疗临床研究内容关键词：

肿瘤靶向治疗基因检测临床应用结果

结直肠癌复发转多基因检测位点研究的目的：结直肠癌复发转多基因检测位点研究探讨结直肠癌外泌体lncRNA前列腺癌相关转录物1-（PCAT1）介导的循环肿瘤及细胞结直肠癌肝转移的机制。结直肠癌复发转多基因检测位点研究的方法：从原发性结直肠癌（CRC）细胞株HCT116和SW480中提取外泌体并与 T84 和人脐静脉内皮 (HUVE) 细胞一起培养。实时定量聚合酶链反应（RT-qPCR）检测PCAT1和miR-329-3p的表达，Western blot检测Netrin-1、CD146和上皮间质转化（EMT）相关蛋白的表达，细胞计数试剂盒8（CCK-8）检测T84细胞增殖活性，Transwell检测细胞迁移。外泌体与人脐静脉内皮细胞 (HUVEC) 共培养后，通过免疫荧光检测 F-肌动蛋白信号的表达。在直肠癌肝转移小鼠模型中观察到基因检测PCAT1缺失后皮下肿瘤和肝结节大小的变化。结直肠癌复发转多基因检测位点研究的结果：PCAT1在原代细胞系及其外泌体中的表达上调。外泌体与结直肠癌肿瘤循环T84细胞共培养后，Netrin-1和CD146基因检测表达上调，miR-329-3p表达下调，T84细胞增殖和迁移能力增强，发生EMT。基因敲除PCAT1后，上述现象发生逆转。同样，外泌体与 HUVECs 共培养后，F-actin 信号的表达增加，而 PCAT1 被敲低后，F-actin 信号也降低。 PCAT1 调节 miR-329-3p/Netrin-1 并影响 HUVECs 中 T84 和 F-肌动蛋白信号表达的生物学行为。在结直肠癌肝转移小鼠模型中，敲除PCAT1可显着减少小鼠肝转移形成的结节。结直肠癌复发转多基因检测位点研究的结论：来源于结直肠癌外泌体的LncRNA PCAT1调节循环肿瘤细胞（CTCs）中Netrin-1-CD146复合物的活性)促进结直肠癌EMT和肝转移的发生，为根据基因检测结果治疗结直肠癌肝转移提供新的分子靶点。

肿瘤发生与复发转移国际数据库描述：

Objective: This study explored the colorectal cancer exosome lncRNA prostate cancer associated transcript 1- (PCAT1) mediated circulating tumors and the mechanism of cell colorectal cancer liver metastasis.Methods: Exosomes were extracted from the primary colorectal cancer (CRC) cell lines HCT116 and SW480 and cultured with T84 and human umbilical vein endothelial (HUVE) cells. The expression of PCAT1 and miR-329-3p was detected by real-time quantitative polymerase chain reaction (RT-qPCR), the expression of Netrin-1, CD146, and epithelial mesenchymal transition (EMT) related proteins was detected by Western blot, the proliferation activity of T84 cells was detected by cell counting kit 8 (CCK-8), and cell migration was detected by Transwell. The expression of the F-actin signal was detected by immunofluorescence after coculture of exosomes with human umbilical vein endothelial cells (HUVECs). Changes in subcutaneous tumor and liver nodule size after PCAT1 deletion were observed in a mouse model of liver metastasis from rectal cancer.Results: PCAT1 expression was upregulated in primary cell lines and their exosomes. After exosomes were cocultured with colorectal cancer tumor circulating T84 cells, the expression of Netrin-1 and CD146 was upregulated, the expression of miR-329-3p was downregulated, the proliferation and migration ability of T84 cells were enhanced, and EMT occurred. After knocking down PCAT1, the above phenomenon was reversed. Similarly, after exosomes were cocultured with HUVECs, the expression of the F-actin signal increased, and after PCAT1 was knocked down, the F-actin signal also decreased. PCAT1 regulates miR-329-3p/Netrin-1 and affects the biological behavior of T84 and F-actin signal expression in HUVECs. In a mouse model of colorectal cancer liver metastasis, knocking down PCAT1 significantly reduced the nodules formed by liver metastasis in mice.Conclusions: LncRNA PCAT1 derived from colorectal cancer exosomes regulates the activity of the Netrin-1-CD146 complex in circulating tumor cells (CTCs) to promote the occurrence of colorectal cancer EMT and liver metastasis and provides new molecular targets for the treatment of colorectal cancer liver metastasis.

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