ArticleOncology reports2026
Effect of the miR‑26a/b‑5p‑STAT3‑YKL‑40 regulatory axis on proliferation, migration, and invasion of endometrial cancer cells.
Article in Oncology reports, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
The incidence of endometrial cancer (EC) is on the rise annually, emphasizing the importance of timely diagnosis and treatment. Signal transducer and activator of transcription 3 (STAT3) has been identified as a proto‑oncogene involved in multiple signaling pathways affecting various biological processes, especially in tumours. The aim of the present study was to validate the impact of STAT3 on EC phenotype and investigate its upstream and downstream regulatory mechanisms. Immunohistochemical analysis was conducted to assess STAT3 expression in EC tissues, followed by dual luciferase assays to confirm the regulatory relationship between STAT3 and microRNA (miR)‑26a/b‑5p. The effects of STAT3 and miR‑26a/b‑5p on HEC‑1A cell proliferation and metastasis were evaluated through Cell Counting Kit‑8 assays, cell scratch assays, and Transwell assays. Co‑immunoprecipitation assays verified the binding between STAT3 and chitinase‑3‑like protein 1 (CHI3L1, also known as YKL‑40). The results demonstrated high STAT3 expression in EC, associated with disease progression. miR‑26a/b‑5p directly targeted STAT3. Upregulated STAT3 enhanced HEC‑1A cell proliferation, migration, and invasion, counteracting the inhibitory effects of miR‑26a/b‑5p on cell migration and invasion. In addition, it was confirmed that STAT3 binds to and promotes the expression of YKL‑40. These findings contribute to clarifying the pathogenesis of EC.
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