LncRNA PSMB8-AS1 contributes to pancreatic cancer progression via modulating miR-382-3p/STAT1/PD-L1 axis

Background Accumulating evidence demonstrates the essential role of long non-coding RNA (lncRNA) in various types of cancers, including pancreatic cancer. However, the functions and regulation mechanism of lncRNA PMSB8-AS1 in pancreatic cancer are largely unclear. Methods Quantitative reverse transc...

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Published in:Journal of experimental & clinical cancer research 2020-09, Vol.39 (1), p.1-179, Article 179
Main Authors: Zhang, Hao, Zhu, Changhao, He, Zhiwei, Chen, Shiyu, Li, Lin, Sun, Chengyi
Format: Article
Language:English
Subjects:
Analysis
Binding sites
Breast cancer
Cancer metastasis
Cancer therapies
Cell adhesion & migration
Cell culture
Cell growth
Cholecystokinin
Development and progression
Epigenetics
Metastasis
miR-382–3p
Pancreatic cancer
PDL1
PMSB8-AS1
Proteins
RNA
STAT1
Surgery
Tumorigenesis
Tumors
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Summary:Background Accumulating evidence demonstrates the essential role of long non-coding RNA (lncRNA) in various types of cancers, including pancreatic cancer. However, the functions and regulation mechanism of lncRNA PMSB8-AS1 in pancreatic cancer are largely unclear. Methods Quantitative reverse transcription PCR (qRT-PCR) is used to examine the expression of PMSB8-AS1 in PC tissues and PC cell lines. The effect of PMSB8-AS1 on the proliferation of PC cells was detected using CCK8 assay, colony assay, and flow cytometry. The effect of PMSB8-AS1 on the migration and invasion of pancreatic cancer cells was detected using a wound-healing assay and transwell migration assay. Bioinformatic analysis, double luciferase reporting assay, western blot, and rescue experiments were used to detect the regulatory relationship between PMSB8-AS1, miR-382-3p, STAT1, and PD-L1. Results PMSB8-AS1 expression was upregulated in PC tissues and cell lines and positively associated with the worst survival in patients with PC. The in vitro and in vivo assays demonstrated that overexpression of PMSB8-AS1 significantly promoted pancreatic cancer cell proliferation, migration, and invasion, whereas knockdown of PMSB8-AS1 suppressed cell proliferation, migration, invasion, and EMT, and decreased apoptosis of PC cells. Besides, PMSB8-AS1 directly bound to miR-382-3p downregulated its expression. Besides, PMSB8-AS1 reversed the effect of miR-382-3p on the growth and metastasis of PC cells, which might be targeted on STAT1. Furthermore, STAT1 is the transcriptional factor that activates the expression of PD-L1. Conclusion lncRNA PMSB8-AS1 promotes pancreatic cancer progression via STAT1 by sponging miR-382-3p involving regulation PD-L1. Keywords: PMSB8-AS1, Pancreatic cancer, PDL1, miR-382-3p, STAT1
ISSN:1756-9966
0392-9078
1756-9966
DOI:10.1186/s13046-020-01687-8