PD‑L1 expression increased by IFN‑γ via JAK2‑STAT1 signaling and predicts a poor survival in colorectal cancer
- Tiancheng Zhao
- Yezhou Li
- Jiayu Zhang
- Bin Zhang
Affiliations: Department of Endoscopy Center, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, Department of Vascular Surgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, Department of Gastrointestinal Colorectal and Anal Surgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
- Published online on: May 20, 2020 https://doi.org/10.3892/ol.2020.11647
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PD‑L1 inhibitors are widely used in tumor immunotherapy, but their mechanism in colorectal cancer remains unclear. The present study aimed to investigate the mechanisms underlying programmed death ligand 1 (PD‑L1) regulation via the interferon‑γ (IFN‑γ)/janus kinase (JAK)/STAT signaling pathway, and its prognostic value in patients with colorectal cancer (CRC). A cohort of 181 patients were recruited to determine the association between PD‑L1 expression and CRC prognosis; the patients were newly diagnosed with colorectal adenocarcinoma and had also undergone a physical tumorectomy. Immunohistochemical staining and survival analysis were used to evaluate the predictive value of PD‑L1 protein expression in CRC. Gene set enrichment analysis, RT‑qPCR and western blotting, etc were performed to confirm that PD‑L1 is regulated by the IFN‑γ/JAK/STAT signaling pathway. PD‑L1 up‑regulation was more frequently observed in patients with larger tumors, positive vascular or lymphatic infiltration and a poorly differentiated stage in addition to being associated with a poor survival in patients with CRC. Following the stimulation with IFN‑γ, PD‑L1 expression levels were revealed to be increased via the JAK2/STAT1 signaling pathway. In conclusion, the findings of the present study indicated that the expression levels of PD‑L1 may be associated with a poor prognosis in patients with CRC. In addition, the results suggested that the IFN‑γ‑mediated overexpression of PD‑L1 in CRC cells may be regulated by the JAK2/STAT1 signaling pathway.