{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have revealed that in the tumor microenvironment of endometrial cancer, the long non‐coding RNA NIFK‐AS1 is significantly downregulated in tumor‐associated macrophages, a cell type known to influence tumor progression. This decreased expression is associated with a concomitant increase in miR-146a levels, suggesting that NIFK-AS1 normally plays a role in maintaining proper macrophage function."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFunctional experiments demonstrated that overexpressing NIFK-AS1 in macrophages suppresses the IL-4-induced polarization toward the M2 phenotype. Mechanistically, NIFK-AS1 acts as a molecular sponge for miR-146a, thereby relieving the repression of Notch1 expression. This regulatory interaction is critical because it diminishes the pro-tumorigenic M2-like polarization, which is known to support tumor growth."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, the enforced expression of NIFK-AS1 not only modulates macrophage behavior but also inhibits the 17β-estradiol-induced proliferation, migration, and invasion of endometrial cancer cells. These findings underscore the dual role of NIFK-AS1 as both an immune modulator and a suppressor of malignant cell behavior, highlighting its potential as a novel therapeutic target in managing endometrial cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yun-Xiao Zhou, Wei Zhao, Li-Wei Mao, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long non-coding RNA NIFK-AS1 inhibits M2 polarization of macrophages in endometrial cancer through targeting miR-146a."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Biochem Cell Biol (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.biocel.2018.08.017"}], "href": "https://doi.org/10.1016/j.biocel.2018.08.017"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30176290"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30176290"}]}]}]}