Abstract
Background
Endometriosis (EM) is a prevalent gynecological condition whose etiology remains incompletely understood. This study aimed to investigate the potential mechanisms of LINC01315 in EM.
Methods
This study recruited 150 EM patients and 150 healthy controls, with RT-qPCR used to detect the relative expression of target molecules. Cell proliferation, migration, and invasion were assessed using CCK-8 and Transwell assays, respectively. Inflammatory cytokines were quantified via ELISA. The targeted interaction between miR-497-5p and LINC01315/BDNF was validated through RIP and dual luciferase assays. Functional networks downstream of miR-497-5p were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway databases.
Results
LINC01315 exhibited significantly elevated expression in EM, correlating with progressively higher visual analogue scale (VAS) scores of dysmenorrhea and revised American Society for Reproductive Medicine (rASRM) staging, demonstrating strong diagnostic efficacy. LINC01315 knockdown markedly suppressed the proliferation, migration, and invasion of hEM15A cells. It also reduced the expression and secretion of key inflammatory factors, including IL-6, TNF-α, and IL-1β. Mechanistically, LINC01315 targeted miR-497-5p. In EM patients, miR-497-5p was downregulated while BDNF expression was elevated. Furthermore, miR-497-5p specifically suppressed BDNF expression. Functional experiments confirmed that miR-497-5p inhibitors reversed the inhibitory effects of LINC01315 knockdown on the malignant phenotype and inflammatory cytokine secretion in hEM15A cells, while re-knocking down BDNF reinstated the inhibitory effects.
Conclusion
LINC01315 promoted EM progression by adsorbing miR-497-5p and relieving its inhibition on BDNF.
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Acknowledgements
Not Applicable.
Funding
The therapeutic effect and research of Guizhi Fuling Pill combined with Leuprorelin Acetate in endometriosis (No.ZF2024232).
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The study protocol was approved by the Ethics Committee of The Second Hospital of Jingzhou and followed the principles outlined in the Declaration of Helsinki. In addition, informed consent has been obtained from the participants involved.
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The authors declare no competing interests.
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Supplementary Information
12905_2026_4853_MOESM1_ESM.tif (download TIF )
Supplementary Material 1: Supplementary Fig. 1. Subcellular localization of LINC01315 in hEM15A cells. LINC01315 was predominantly cytoplasmic (~ 78%). U6 was predominantly nuclear (~ 85%). GAPDH mRNA was predominantly cytoplasmic (~ 88%). Percentages were calculated by the 2−ΔΔCt method. Data were presented as mean ± SD from three independent biological replicates. Statistical analyses were performed using a two‑tailed independent‑samples t‑test.
12905_2026_4853_MOESM2_ESM.tif (download TIF )
Supplementary Material 2: Supplementary Fig. 2. Gain‑of‑function validation of the LINC01315/miR‑497‑5p/BDNF axis in hEM15A cells. A–C. RT‑qPCR validation of overexpression efficiency for LINC01315 (A), miR‑497‑5p mimic (B), and BDNF (C) in hEM15A cells compared with OE‑NC controls. D–E. RT‑qPCR analysis showing that LINC01315 overexpression suppressed miR‑497‑5p expression while upregulating BDNF; co‑transfection with miR‑497‑5p mimic reversed these effects (D), and co‑transfection with OE‑BDNF restored BDNF expression (E). F. CCK‑8 assay demonstrating that LINC01315 overexpression enhanced cell proliferation, which was antagonized by miR‑497‑5p mimic and rescued by BDNF overexpression. G. Transwell migration and invasion assays showing that LINC01315 overexpression promoted cell migration and invasion, reversed by miR‑497‑5p mimic and restored by BDNF overexpression. H–I. RT‑qPCR (H) and ELISA (I) analyses revealing that LINC01315 overexpression upregulated mRNA and secreted protein levels of IL‑6, TNF‑α, and IL‑1β; these effects were alleviated by miR‑497‑5p mimic and reinstated by BDNF overexpression. Data were presented as mean ± SD from five independent biological replicates. **P < 0.01, ***P < 0.001. Statistical analyses were performed using one‑way ANOVA with Bonferroni post‑hoc test.
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Supplementary Material 3: Supplementary Fig. 3. Normal Q-Q plots of relative expression (2⁻ΔΔCt) for three serum biomarkers. Each subplot displays the expected values of a standard normal distribution (vertical axis) against the measured relative expression values (horizontal axis) of LINC01315, miR-497-5p, and BDNF, respectively. Data points of all three biomarkers closely align with the theoretical diagonal reference line, visually verifying that the expression data conform to a normal distribution, which supports the application of Pearson correlation analysis.
12905_2026_4853_MOESM4_ESM.tif (download TIF )
Supplementary Material 4: Supplementary Fig. 4. Western blot results showing total and phosphorylated AKT/mTOR expression. β-actin served as internal reference.
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Ma, H., Yu, H., Wang, Q. et al. Long non-coding RNA LINC01315 accelerates the development of endometriosis through the miR-497-5p/BDNF axis. BMC Women's Health (2026). https://doi.org/10.1186/s12905-026-04853-w
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DOI: https://doi.org/10.1186/s12905-026-04853-w
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