Peptidase inhibitor 16 promotes proliferation of pancreatic ductal adenocarcinoma cells through OASL signaling.

Autor: Chen Q; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China., Jiang LY; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China., Cao C; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China., Liu FY; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China., Li DR; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China., Wu PF; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China., Jiang KR; Pancreas Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jazyk: angličtina
Zdroj: Molecular carcinogenesis [Mol Carcinog] 2024 May; Vol. 63 (5), pp. 938-950. Date of Electronic Publication: 2024 Feb 14.
DOI: 10.1002/mc.23699
Abstrakt: Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive cancer with a poor prognosis and a 5-year survival rate of less than 11%. As a member of the CAP superfamily of proteins, the role of peptidase inhibitor 16 (Pi16) in tumor progression is still unclear. Immunohistochemistry and quantitative RT-PCR methods were used to detect the expression levels of Pi16 protein and mRNA in PDAC patients. CRISPR/Cas9 technology was used to knock out the expression of Pi16 in PDAC cell lines. In vivo and in vitro experiments were used to verify the effect of Pi16 on PDAC proliferation ability. By RNA sequencing, we found that oligoadenylate synthetase L (OASL) can serve as a potential downstream target of Pi16. The expression of Pi16 was higher in PDAC tissues than in matched adjacent tissues. High expression of Pi16 was associated with PDAC progression and poor prognosis. Overexpression of Pi16 could promote the proliferation of PDAC cells in vitro and in vivo. Bioinformatics analysis and coimmunoprecipitation assays showed that Pi16 could bind to OASL. Moreover, the functional recovery test confirmed that Pi16 could promote the proliferation of PDAC via OASL. Our present study demonstrates that Pi16 might participate in the occurrence and development of PDAC by regulating cell proliferation by binding to OASL, indicating that Pi16 might be a promising novel therapeutic target for PDAC.
(© 2024 Wiley Periodicals LLC.)
Databáze: MEDLINE
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