PDF(Pubmed)
Abstract：
Collagen type XI α1 (COL11A1) is associated with tumorigenesis and development in many human malignancies. Previous reports indicate that COL11A1 may be a significant diagnostic marker for pancreatic ductal adenocarcinoma (PDAC); however, its biological role in PDAC progression remains unclear. In this study, we investigated the influence of COL11A1 on the invasion and migration abilities of pancreatic cancer cells and explored its potential molecular mechanisms.
Cell migration and invasion were assessed using Transwell assays in pancreatic cancer cells transfected with siCOL11A1 and pCNV3-COL11A1 plasmids. The protein and mRNA expression levels of N-cadherin, E-cadherin, Vimentin, cluster of differentiation (CD)-24, CD44, serine-threonine kinase (AKT), glycogen synthase kinase (GSK)-3β, phospho (p)-AKTSer473, p-GSK-3βSer9, and Snail were analyzed using Western blotting and real-time polymerase chain reaction (PCR). The effect of COL11A1 on cell stemness was tested using flow cytometry and clone formation assays.
These results demonstrated that COL11A1 significantly promoted the invasion and migration abilities of PDAC cells. Furthermore, COL11A1 facilitated the occurrence of epithelial-mesenchymal transition (EMT) and cell stemness by upregulating the expression levels of p-AKTSer473, p-GSK-3βSer9, and Snail.
This study suggests that the activation of the AKT/GSK-3β/Snail signaling pathway induced by COL11A1 plays a major role in the progression of PDAC. Therefore, COL11A1 could serve as a potential target for PDAC treatment.
Cell migration and invasion were assessed using Transwell assays in pancreatic cancer cells transfected with siCOL11A1 and pCNV3-COL11A1 plasmids. The protein and mRNA expression levels of N-cadherin, E-cadherin, Vimentin, cluster of differentiation (CD)-24, CD44, serine-threonine kinase (AKT), glycogen synthase kinase (GSK)-3β, phospho (p)-AKTSer473, p-GSK-3βSer9, and Snail were analyzed using Western blotting and real-time polymerase chain reaction (PCR). The effect of COL11A1 on cell stemness was tested using flow cytometry and clone formation assays.
These results demonstrated that COL11A1 significantly promoted the invasion and migration abilities of PDAC cells. Furthermore, COL11A1 facilitated the occurrence of epithelial-mesenchymal transition (EMT) and cell stemness by upregulating the expression levels of p-AKTSer473, p-GSK-3βSer9, and Snail.
This study suggests that the activation of the AKT/GSK-3β/Snail signaling pathway induced by COL11A1 plays a major role in the progression of PDAC. Therefore, COL11A1 could serve as a potential target for PDAC treatment.
摘要：
XI型胶原α1（COL11A1）与许多人类恶性肿瘤的肿瘤发生和发展有关。以前的报告表明，COL11A1可能是胰腺导管腺癌（PDAC）的重要诊断标志物；然而，其在PDAC进展中的生物学作用尚不清楚.在这项研究中,我们研究了COL11A1对胰腺癌细胞侵袭和迁移能力的影响，并探讨了其潜在的分子机制。
使用Transwell测定在用siCOL11A1和pCNV3-COL11A1质粒转染的胰腺癌细胞中评估细胞迁移和侵袭。N-cadherin的蛋白和mRNA表达水平,E-cadherin,Vimentin,分化簇（CD）-24，CD44，丝氨酸-苏氨酸激酶（AKT），糖原合成酶激酶(GSK)-3β,使用蛋白质印迹和实时聚合酶链反应（PCR）分析磷酸（p）-AKTSer473，p-GSK-3βSer9和Snail。使用流式细胞术和克隆形成测定法测试了COL11A1对细胞干性的影响。
这些结果表明COL11A1显著促进PDAC细胞的侵袭和迁移能力。此外，COL11A1通过上调p-AKTSer473，p-GSK-3βSer9和Snail的表达水平，促进了上皮间质转化（EMT）和细胞干性的发生。
这项研究表明，由COL11A1诱导的AKT/GSK-3β/Snail信号通路的激活在PDAC的进展中起主要作用。因此,COL11A1可以作为PDAC治疗的潜在靶标。
使用Transwell测定在用siCOL11A1和pCNV3-COL11A1质粒转染的胰腺癌细胞中评估细胞迁移和侵袭。N-cadherin的蛋白和mRNA表达水平,E-cadherin,Vimentin,分化簇（CD）-24，CD44，丝氨酸-苏氨酸激酶（AKT），糖原合成酶激酶(GSK)-3β,使用蛋白质印迹和实时聚合酶链反应（PCR）分析磷酸（p）-AKTSer473，p-GSK-3βSer9和Snail。使用流式细胞术和克隆形成测定法测试了COL11A1对细胞干性的影响。
这些结果表明COL11A1显著促进PDAC细胞的侵袭和迁移能力。此外，COL11A1通过上调p-AKTSer473，p-GSK-3βSer9和Snail的表达水平，促进了上皮间质转化（EMT）和细胞干性的发生。
这项研究表明，由COL11A1诱导的AKT/GSK-3β/Snail信号通路的激活在PDAC的进展中起主要作用。因此,COL11A1可以作为PDAC治疗的潜在靶标。
