Long non-coding RNA LINC01315 accelerates the development of endometriosis through the miR-497-5p/BDNF axis

In: BMC Women's Health · 2026 · doi:10.1186/s12905-026-04853-w · W7213897085
OA: gold CC0
⚙ AI-generated summary by qwen3.7-flash, 2026-09-23 ⓘ

Elevated LINC01315 promotes endometriosis progression by sponging miR-497-5p to relieve its inhibition on BDNF, thereby enhancing cell proliferation, migration, invasion, and inflammatory cytokine secretion.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by qwen3.7-flash, 2026-09-23 · read from full text ⓘ

This study investigated the role of long non-coding RNA LINC01315 in endometriosis by analyzing tissue samples from 150 patients and 150 healthy controls alongside in vitro experiments on hEM15A cells. The researchers found that LINC01315 expression was significantly elevated in endometriosis lesions and correlated with disease severity, while its knockdown suppressed cell proliferation, migration, invasion, and inflammatory cytokine secretion. Mechanistically, LINC01315 acted as a sponge for miR-497-5p, thereby relieving the inhibition of Brain-Derived Neurotrophic Factor (BDNF) to promote disease progression. This paper is centrally about endometriosis — specifically elucidating a molecular pathway involving lncRNA, microRNA, and neurotrophic factors that drive lesion development.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis (EM) is a prevalent gynecological condition whose etiology remains incompletely understood. This study aimed to investigate the potential mechanisms of LINC01315 in EM. 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. 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. LINC01315 promoted EM progression by adsorbing miR-497-5p and relieving its inhibition on BDNF .
Full text 6,733 characters · extracted from oa-html · 5 sections · click to expand

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. Similar content being viewed by others

Acknowledgements

Not Applicable. Funding The therapeutic effect and research of Guizhi Fuling Pill combined with Leuprorelin Acetate in endometriosis (No.ZF2024232). Author information Authors and Affiliations Corresponding author Ethics declarations Ethics approval and consent to participate 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. Consent for publication Not applicable. Competing interests The authors declare no competing interests. Additional information Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. 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. 12905_2026_4853_MOESM3_ESM.tif (download TIF ) 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. Rights and permissions Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/. About this article Cite this article 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 Received: Accepted: Published: DOI: https://doi.org/10.1186/s12905-026-04853-w

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-html ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2026) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

openalex
last seen: 2026-10-09T06:00:51.939507+00:00
License: CC0 · commercial use OK