Research Paper Volume 16, Issue 16 pp 12063—12072
Mechanistic study of PD-L1 regulation of metastatic proliferation in non-small cell lung cancer through modulation of IRE1α/XBP-1 signaling pathway in tumor-associated macrophages
- 1 Department of Radiation Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, China
Received: February 10, 2024 Accepted: August 2, 2024 Published: August 24, 2024
https://doi.org/10.18632/aging.206082How to Cite
Copyright: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Objective: To explore the related research of PD-L1 in IRE1α/XBP-1 signaling pathway on non-small cell lung cancer.
Methods: The tumor model of mice was established and divided into four groups; after successful modeling, the tumor tissue of mice was removed for subsequent experiments; the bought THP-1 cells were grouped into four different groups, a control group, nivolumab intervention group, IRE1α inhibition group, and nivolumab intervention + IRE1α inhibition group; after co-culture of the four groups of THP-1 cells with A549, THP-1 cell protein levels in the four groups were analyzed using Western blot; A549 cell migration, invasion and proliferation were assessed using the scratch assay, Transwell method, monoclonal experiment and CCK-8 method.
Results: In vivo studies indicated that the stimulation of nivolumab could strongly check the progress of NSCLC (non-small cell lung); two groups treated with 4 μ8c showed obvious effects on check point of NSCLC; In vitro experiments including Western-blot experiment, Scratch experiment, Transwell method, Monoclonal experiment and CCK-8 experiment suggest that nivolumab could inhibit migration, invasion and proliferation of NSCLC tumor cells and it.
Conclusion: PD-L1 is capable of controlling metastatic and proliferative potential of NSCLC by the way of the modification of IRE1α/XBP-1 signaling in tumor-associated macrophages.