ArticleHereditas2026
Mechanistic insights into miR-4775-mediated regulation of pancreatic cancer cell invasion and migration through BRMS1L.
Article in Hereditas, 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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Authors and funding
5 authors.
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Abstract
BACKGROUND AND
aimsThis study aims to investigate the effects of miR-4775 on pancreatic cancer cell (PC) invasion and migration, and to elucidate the underlying molecular mechanisms.
methodsQuantitative Real-Time Reverse Transcription (RT-qPCR) was performed to analyze miR-4775 and BRMS1L expression levels in both human PC tissues and human pancreatic carcinoma cells (PANC-1) lines. The prognostic value of miR-4775 in PC patients was evaluated through survival analysis. The CCK-8 assay was employed to assess cell viability, while Transwell assays were utilized to evaluate invasion and migration capabilities. The regulatory interaction between miR-4775 and BRMS1L was confirmed by dual-luciferase reporter assay.
resultsComparative analysis revealed significantly elevated miR-4775 expression in PC tissues versus adjacent normal tissues, with high miR-4775 expression correlating with poorer patient prognosis. Functional studies demonstrated that inhibition of miR-4775 significantly attenuated cellular viability, migration, and invasion capabilities, while knockdown of breast cancer metastasis suppressor 1-like (BRMS1L) effectively rescued these suppressive effects. The luciferase reporter assay confirmed a direct negative regulatory relationship between miR-4775 and its target gene BRMS1L.
conclusionsThese findings demonstrate that miR-4775 regulates PC progression by modulating cancer cell viability, migration, and invasion through BRMS1L-mediated mechanisms.
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