Related Experiment Video
Updated: Jul 12, 2025
Generation of Orthotopic Pancreatic Tumors and Ex vivo Characterization of Tumor-Infiltrating T Cell Cytotoxicity
Published on: December 7, 2019
High expression ITGA2 affects the expression of MET, PD-L1, CD4 and CD8 with the immune microenvironment in
Liquan Jin1, Yaoqiang Duan2, Xiaoxi Li2
11St Department of General Surgery, The First Affiliated Hospital of Dali University, Dali, Yunnan, China.
Purpose:
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.
Experimental Design:
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.
Results:
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.
Conclusions:
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.
Insights
ITGA2 promotes pancreatic cancer growth and invasion by upregulating MET and PD-L1. Targeting ITGA2 offers a promising strategy to improve immunotherapy efficacy and inhibit tumor progression in pancreatic cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Pancreatic cancer presents a significant clinical challenge due to its poor prognosis.
- Integrin alpha 2 (ITGA2) is frequently overexpressed in various tumor tissues and is a potential therapeutic target.
Purpose of the Study:
- To investigate the expression of ITGA2, epithelial-mesenchymal transition (EMT), and programmed death-ligand 1 (PD-L1) in pancreatic cancer.
- To elucidate the role of ITGA2 in pancreatic cancer progression and its correlation with EMT and PD-L1.
Main Methods:
- Immunofluorescence and immunohistochemistry were employed to assess protein expression in 62 pancreatic cancer samples.
- Functional assays (cell migration, transwell) and molecular analyses (Western blot, RT-qPCR) were utilized to determine ITGA2's biological role and regulatory mechanisms.
Main Results:
- ITGA2, E-cadherin, and PD-L1 were expressed in both tumor and stroma of pancreatic cancer, with significant positive correlations.
- Elevated ITGA2, CD4, and CD8 expression in tumor tissues correlated with poorer patient survival.
- Blocking ITGA2 significantly inhibited pancreatic cancer cell proliferation and invasion, downregulating EMT and PD-L1.
Conclusions:
- ITGA2 plays a critical role in regulating pancreatic cancer growth and invasion, partly through MET and PD-L1 upregulation.
- Increased ITGA2 expression is linked to poor prognosis and affects immune regulation in pancreatic cancer.
- Targeting ITGA2 represents a viable strategy to enhance checkpoint immunotherapy and combat pancreatic cancer growth.
More Related Videos
07:55Flow Cytometry-Based Isolation and Therapeutic Evaluation of Tumor-Infiltrating Lymphocytes in a Mouse Model of Pancreatic Cancer
Published on: January 17, 2025
08:30Immunophenotyping of Orthotopic Homograft Syngeneic of Murine Primary KPC Pancreatic Ductal Adenocarcinoma by Flow Cytometry
Published on: October 9, 2018