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ABSTRACT
Pumilio RNA-binding family member 1 (PUM1) has been implicated in both the progression of colorectal cancer and the regulation of inflammation. The role of PUM1 in the polarization of tumor-associated macrophages (TAMs) into the M2 phenotype has not yet been reported in hepatocellular carcinoma. Using the PUM1-knockout mice model, flow cytometry, and IHC, we validated the role of PUM1 in hepatocellular carcinoma (HCC) TAMs. One-way analysis of variance (ANOVA) or student’s t-tests was used to compare the experimental groups. We found that PUM1 inhibited anti-tumor immunity in HCC through TAM-mediated inhibition of CD8+ T cells. We also showed that PUM1 promotes the transformation of TAMs into pro-tumorigenic M2-like phenotypes by activating cAMP signaling pathway. This study emphasized the potential of PUM1 as a target for immunotherapy in HCC through TAMs. The present study revealed the molecular mechanism underlying the pro-tumor role of PUM1 in HCC.
Acknowledgements
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Disclosure statement
No potential conflict of interest was reported by the author(s).
Author contributions
Liu Ouyang and Chen-ming Ni designed the study. All of the authors were involved in conducting the experiment, data analysis, and writing the manuscript. All of the authors revised the manuscript. All of the authors studied and approved the final manuscript.
Availability of data and materials
The data used for the current study will be available from the corresponding authors upon reasonable request.
Supplemental material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/15384101.2024.2355825