ArticleAmerican journal of translational research2026
Inhibiting OAS3 suppresses the development of clear cell renal cell carcinoma by reducing cell proliferation and altering the tumor immune microenvironment.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundImmune checkpoint inhibitors have been approved for first-line treatment of metastatic clear cell renal cell carcinoma (ccRCC), but limited therapeutic effects have been reported in patients with advanced ccRCC. Investigating vital targets in specific immune interactions and their effect on the tumor microenvironment of ccRCC could provide novel strategies for overcoming the above limitations.
methodsWe investigated the expression characteristics, prognostic role, and immune associations of OAS3 in the tumor microenvironment in patients with ccRCC. The functions of OAS3 in proliferation and migration were explored in 786-O and OS-RC-2 cells by forced OAS3 overexpression or knockdown. Furthermore, a xenograft model was established in C57BL/6 mice to study the combined effects of OAS3 downregulation and anti-PD1 therapy. The growth, proliferation, and apoptosis of tumor cells, as well as the infiltration of CD8+ T cells and M1/M2 macrophages within tumor tissues, were evaluated by immunohistochemistry.
resultsOAS3 was upregulated in ccRCC and significantly associated with the overall survival of patients with ccRCC. OAS3 expression levels were correlated with genomic mutation profiles and were positively associated with the infiltration of CD8+ T cells, macrophages, neutrophils, and dendritic cells. OAS3 upregulation increased the proliferation, migration, invasion, and colony formation abilities of 786-O and OS-RC-2 cells. In contrast, OAS3 knockdown had the opposite effect.
conclusionOAS3 is upregulated in ccRCC and promotes tumor progression by mediating the infiltration of immune cells in the TME. OAS3 represents a promising therapeutic target for enhancing the antitumor effects of immune checkpoint inhibitors.
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