■胰腺癌的特征是预后不良,被认为是最可怕的恶性肿瘤之一。在不同肿瘤组织中显示高表达的基因中,ITGA2是癌症治疗的有希望的候选者。在胰腺癌中促进癌症是无效的。这项研究的目的是评估胰腺癌中ITGA2,EMT和PD-L1的存在。
■我们检查了ITGA2,MET,E-cadherin,使用多组织免疫荧光和免疫组织化学技术在62个胰腺癌组织样本中的PD-L1,CD4和CD8蛋白。功能测定,如细胞迁移测定和transwell测定,用于确定ITGA2在胰腺癌中的生物学作用。使用Westernblot分析和RT-qPCR检测ITGA2,EMT和PD-L1的关系。
■在我们的研究中,我们观察到ITGA2,E-cadherin,PD-L1在胰腺癌肿瘤和间质组织中的表达。此外,ITGA2、E-cadherin、和PD-L1在肿瘤区域(r=0.559,P<0.001和r=0.511,P<0.001),间质区PD-L1(r=0.512,P<0.001)。胰腺癌组织中ITGA2、CD4和CD8的表达水平高于癌旁组织(P<0.05)。此外,ITGA2与CD4、CD8呈负相关(r=-0.344,P<0.005,r=-0.398,P<0.005)。此外,发现ITGA2、CD4和CD8与患者的生存时间相关(P<0.05)。阻断ITGA2显著抑制胰腺癌细胞的增殖和侵袭能力,此外,sh-ITGA2可以下调EMT和PD-L1的表达。
■我们发现了一种新的机制,其中ITGA2在调节胰腺癌的生长和侵袭中起着至关重要的作用。该机制涉及胰腺癌细胞中MET和PD-L1表达的上调。此外,我们发现,在胰腺癌患者中,ITGA2表达增加与预后不良相关.此外,ITGA2也影响这些患者的免疫调节。因此,靶向ITGA2是增强检查点免疫疗法疗效和阻止肿瘤生长的有效方法。
Pancreatic cancer is characterized by a grim prognosis and is regarded as one of the most formidable malignancies. Among the genes exhibiting high expression in different tumor tissues,
ITGA2 stands out as a promising candidate for cancer therapy. The promotion of cancer in pancreatic cancer is not effective. The objective of this study is to assess the presence of
ITGA2, EMT and PD-L1 in pancreatic cancer.
We examined the expression of ITGA2, MET, E-cadherin, PD-L1, CD4, and CD8 proteins in 62 pancreatic cancer tissue samples using multi-tissue immunofluorescence and immunohistochemistry techniques. Functional assays, such as the cell migration assay and transwell assay, were used to determine the biological role of ITGA2 in pancreatic cancer. The relationship of
ITGA2,EMT and PD-L1 were examined using Western blot analysis and RT-qPCR assay.
In our study, we observed the expression of ITGA2, E-cadherin, and PD-L1 in both tumor and stroma tissues of pancreatic cancer. Additionally, a positive correlation between ITGA2, E-cadherin, and PD-L1 in the tumor region (r=0.559, P<0.001 and r=0.511, P<0.001), and PD-L1 in the stroma region (r=0.512, P<0.001).The expression levels of ITGA2, CD4, and CD8 were found to be higher in pancreatic cancer tissues compared to adjacent tissues (P < 0.05). Additionally, ITGA2 was negatively correlated with CD4 and CD8 (r = -0.344, P < 0.005 and r = -0.398, P < 0.005).Furthermore, ITGA2, CD4, and CD8 were found to be correlated with the survival time of patients (P < 0.05). Blocking ITGA2 inhibited the proliferation and invasion ability of pancreatic cancer cells significantly, Additionally, sh-
ITGA2 can down-regulate the expression of EMT and PD-L1.
We identified a novel mechanism in which ITGA2 plays a crucial role in the regulation of pancreatic cancer growth and invasion. This mechanism involves the upregulation of MET and PD-L1 expression in pancreatic cancer cells. Additionally, we found that increased expression of ITGA2 is associated with a poor prognosis in pancreatic cancer patients. Furthermore,
ITGA2 also affects immune regulation in these patients. Therefore, targeting ITGA2 is an effective method to enhance the efficacy of checkpoint immunotherapy and prohibiting tumor growth against pancreatic cancer.