Translational cancer research · 2026
LINC01614 favors breast cancer progression through the regulation of miR-217/FN1 and mediation in PI3K/AKT signal pathway.
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Ping Ding, Wang Jiaxin, Li Dengfeng, Fang Lin
Аннотация
BACKGROUND: Breast cancer (BC) is the most prevalent malignant tumor and represents a significant threat to women's health. Long non-coding RNAs (LncRNAs), which are RNA molecules longer than 200 nucleotides, have been shown to play critical roles in the progression of BC. Therefore, this study was aimed to explore the function and potential mechanism of LINC01614 in BC, so that it could provide new strategies for future BC therapy.
METHODS: This study used the TANRIC and ENCORI databases to evaluate LINC01614 expression and its prognostic significance. Cell Counting Kit-8 (CCK-8), wound healing, Transwell, and apoptosis assays were conducted to assess its biological function in BC cells. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and Western blot (WB) were employed to explore the molecular mechanisms involved. Enzyme-linked immunosorbent assay (ELISA) detection and in vivo experiments further clarified its role in BC.
RESULTS: The expression of LINC01614 was significantly elevated in BC and correlated with poor prognosis. Elevated LINC01614 expression enhanced BC cell proliferation, migration, and invasion, whereas its knockdown decreased cell viability, inhibited migration and invasion, and triggered apoptosis. Gene expression analysis after LINC01614 knockdown revealed changes in miR-217, FN1, PI3K, AKT, and PTEN levels. Additionally, co-silencing LINC01614 and miR-217 significantly affected PI3K, AKT, PTEN, and FN1 expression. Luciferase assays confirmed direct regulatory interactions between LINC01614 and miR-217, as well as between miR-217 and FN1. Metabolic analysis indicated that LINC01614 knockdown enhanced cellular energy metabolism.
CONCLUSIONS: These results indicate that LINC01614 facilitates BC progression by regulating the PI3K/AKT signaling pathway through miR-217/FN1. Targeting LINC01614 may provide new therapeutic strategies for BC treatment.
METHODS: This study used the TANRIC and ENCORI databases to evaluate LINC01614 expression and its prognostic significance. Cell Counting Kit-8 (CCK-8), wound healing, Transwell, and apoptosis assays were conducted to assess its biological function in BC cells. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and Western blot (WB) were employed to explore the molecular mechanisms involved. Enzyme-linked immunosorbent assay (ELISA) detection and in vivo experiments further clarified its role in BC.
RESULTS: The expression of LINC01614 was significantly elevated in BC and correlated with poor prognosis. Elevated LINC01614 expression enhanced BC cell proliferation, migration, and invasion, whereas its knockdown decreased cell viability, inhibited migration and invasion, and triggered apoptosis. Gene expression analysis after LINC01614 knockdown revealed changes in miR-217, FN1, PI3K, AKT, and PTEN levels. Additionally, co-silencing LINC01614 and miR-217 significantly affected PI3K, AKT, PTEN, and FN1 expression. Luciferase assays confirmed direct regulatory interactions between LINC01614 and miR-217, as well as between miR-217 and FN1. Metabolic analysis indicated that LINC01614 knockdown enhanced cellular energy metabolism.
CONCLUSIONS: These results indicate that LINC01614 facilitates BC progression by regulating the PI3K/AKT signaling pathway through miR-217/FN1. Targeting LINC01614 may provide new therapeutic strategies for BC treatment.