【佳學基因檢測】外泌體基因檢測 lncRNA PCAT1 揭示miR-329-3p/Netrin-1-CD146 復合物是腫瘤循環(huán)細胞介導的結直腸癌肝轉(zhuǎn)移的藥物治療靶點

品牌基因檢測價格表2022年合理性

學習腫瘤基因組學個性化藥物選擇知悉《J Immunol Res》在.?2022 Aug 31;2022:9916228.發(fā)表了一篇題目為《外泌體基因檢測 lncRNA PCAT1 揭示miR-329-3p/Netrin-1-CD146 復合物是腫瘤循環(huán)細胞介導的結直腸癌肝轉(zhuǎn)移的藥物治療靶點》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Xingbao Fang,?Yongping Xu,?Kezhi Li,?Peiwan Liu,?Hong Zhang,?Yang Jiang,?Jianwei Tang,?Yuehong Li?等完成。促進了腫瘤的正確治療與個性化用藥的發(fā)展，進一步強調(diào)了基因信息檢測與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究內(nèi)容關鍵詞：

腫瘤靶向治療基因檢測臨床應用結果

結直腸癌反復轉(zhuǎn)多基因檢測位點研究的目的：結直腸癌反復轉(zhuǎn)多基因檢測位點研究探討結直腸癌外泌體lncRNA前列腺癌相關轉(zhuǎn)錄物1-（PCAT1）介導的循環(huán)腫瘤及細胞結直腸癌肝轉(zhuǎn)移的機制。結直腸癌反復轉(zhuǎn)多基因檢測位點研究的方法：從原發(fā)性結直腸癌（CRC）細胞株HCT116和SW480中提取外泌體并與 T84 和人臍靜脈內(nèi)皮 (HUVE) 細胞一起培養(yǎng)。實時定量聚合酶鏈反應（RT-qPCR）檢測PCAT1和miR-329-3p的表達，Western blot檢測Netrin-1、CD146和上皮間質(zhì)轉(zhuǎn)化（EMT）相關蛋白的表達，細胞計數(shù)試劑盒8（CCK-8）檢測T84細胞增殖活性，Transwell檢測細胞遷移。外泌體與人臍靜脈內(nèi)皮細胞 (HUVEC) 共培養(yǎng)后，通過免疫熒光檢測 F-肌動蛋白信號的表達。在直腸癌肝轉(zhuǎn)移小鼠模型中觀察到基因檢測PCAT1缺失后皮下腫瘤和肝結節(jié)大小的變化。結直腸癌反復轉(zhuǎn)多基因檢測位點研究的結果：PCAT1在原代細胞系及其外泌體中的表達上調(diào)。外泌體與結直腸癌腫瘤循環(huán)T84細胞共培養(yǎng)后，Netrin-1和CD146基因檢測表達上調(diào)，miR-329-3p表達下調(diào)，T84細胞增殖和遷移能力增強，發(fā)生EMT?；蚯贸齈CAT1后，上述現(xiàn)象發(fā)生逆轉(zhuǎn)。同樣，外泌體與 HUVECs 共培養(yǎng)后，F(xiàn)-actin 信號的表達增加，而 PCAT1 被敲低后，F(xiàn)-actin 信號也降低。 PCAT1 調(diào)節(jié) miR-329-3p/Netrin-1 并影響 HUVECs 中 T84 和 F-肌動蛋白信號表達的生物學行為。在結直腸癌肝轉(zhuǎn)移小鼠模型中，敲除PCAT1可顯著減少小鼠肝轉(zhuǎn)移形成的結節(jié)。結直腸癌反復轉(zhuǎn)多基因檢測位點研究的結論：來源于結直腸癌外泌體的LncRNA PCAT1調(diào)節(jié)循環(huán)腫瘤細胞（CTCs）中Netrin-1-CD146復合物的活性)促進結直腸癌EMT和肝轉(zhuǎn)移的發(fā)生，為根據(jù)基因檢測結果治療結直腸癌肝轉(zhuǎn)移提供新的分子靶點。

腫瘤發(fā)生與反復轉(zhuǎn)移國際數(shù)據(jù)庫描述：

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.