NDLI: RBM47 promotes cell proliferation and immune evasion by upregulating PDIA6: a novel mechanism of pancreatic cancer progression

Content Provider	Springer Nature : BioMed Central
Author	Ma, Yihui Liu, Enjie Fan, Huijie Li, Chenfei Huang, Pei Cui, Meiying Wang, Zhengyang Zhou, Jing Chen, Kuisheng
Abstract	Background Pancreatic cancer (PC) is a lethal malignancy characterized by poor prognosis and high mortality. We found the highly expressed RNA-binding motif protein 47 (RBM47) in PC progression. The RBM47 expression was negatively correlated with natural killer (NK) cell infiltrate in PC. Moreover, RBM47 was predicted to bind to the 3′-UTR region of Protein Disulfide Isomerase Family A Member 6 (PDIA6), an oncogene of the development of PC. Therefore, we supposed that RBM47 might affect PC progression by regulating PDIA6. Methods Bioinformatics analysis was performed to screen the candidate gene affecting PC progression using public databases. Loss- and gain-of-function effects of RBM47 on cell proliferation, tumor growth, and immune evasion were determined by CCK-8, EdU incorporation, colony formation assays, the xenogeneic tumor model, and co-culture system of PC and NK-92 cells. RBM47-RNA immunoprecipitation (RIP) followed by PCR and dual luciferase reporter assay were used to detect whether RBM47 could interact with the PDIA6 mRNA and how RBM47 would regulate the transcriptional activity of PDIA6, respectively. Simultaneous overexpression of PDIA6 in RBM47 knockdown PC cells was conducted to clarify whether PDIA6 would mediated effects of RBM47. Given the important role of cellular metabolism in cells proliferation and immune evasion, PC cells with RBM47 knockdown were subjected to metabolomics analysis to further investigate how RBM47 regulate PC progression. Results RBM47 overexpression drove PC progression by promoting cell proliferation and xenografted tumor growth. Consistently, our results showed that RBM47 overexpression weakened sensitivity of PC cells to cytotoxic NK cells. However, RBM47 knockdown exhibited the opposite effects on proliferation and immune evasion of PC cells. RBM47 was able to bind to the 3′-UTR region of PDIA6, maintained PDIA6 mRNA stability, and increased the PDIA6 expression in PC cells. Rescue experiments supported that PDIA6 overexpression reversed the suppressing effects of RBM47 knockdown on cell proliferation and immune evasion. RBM47 knockdown significantly changed metabolites of PC cells. Conclusions In summary, our findings demonstrate that RBM47 contributes to PC progression, which might be mediated by the upregulated PDIA6 expression and the altered cellular metabolites in PC cells, offering a potential therapeutic target for PC treatment. Graphical Abstract
Related Links	https://translational-medicine.biomedcentral.com/counter/pdf/10.1186/s12967-024-05970-6.pdf
Ending Page	21
Page Count	21
Starting Page	1
File Format	HTM / HTML
ISSN	14795876
DOI	10.1186/s12967-024-05970-6
Journal	Journal of Translational Medicine
Issue Number	1
Volume Number	22
Language	English
Publisher	BioMed Central
Publisher Date	2024-12-31
Access Restriction	Open
Subject Keyword	Biomedicine Medicine Public Health Pancreatic cancer RBM47 PDIA6 Immune evasion Medicine/Public Health
Content Type	Text
Resource Type	Article
Subject	Biochemistry, Genetics and Molecular Biology Medicine
Journal Impact Factor	6.1/2023
5-Year Journal Impact Factor	6.3/2023

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