Open Access

Exploring the regulatory role of Linc00893 in asthenozoospermia: Insights into sperm motility and SSC viability

  • Authors:
    • Hui Lu
    • Dongchuan Xu
    • Liqiang Zhao
    • Hailing Ruan
    • Anguo Wang
    • Jiajia Hu
    • Meifang Xiao
    • Weiying Lu
  • View Affiliations

  • Published online on: December 8, 2023     https://doi.org/10.3892/mmr.2023.13143
  • Article Number: 20
  • Copyright: © Lu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The role of long intergenic noncoding RNA 00893 (Linc00893) in asthenozoospermia (AS) and its impact on sperm motility remains unclear The present study explored the effect of Linc00893 on AS, specifically its effect on sperm motility and its relationship with spermatogonial stem cell (SSC) vitality and myosin heavy chain 9 (MYH9) protein expression. Linc00893 expression was analyzed in semen samples using reverse transcription‑quantitative PCR, revealing a significant downregulation in samples from individuals with AS compared with those from healthy subjects. This downregulation was found to be negatively correlated with parameters of sperm motility. To further understand the role of Linc00893, small interfering RNA was used to knockdown its expression in SSCs. This knockdown led to a marked decrease in cell vitality and an increase in apoptosis. Notably, Linc00893 knockdown was shown to inhibit MYH9 expression by competitively binding with microRNA‑107, a finding verified by dual‑luciferase reporter and RNA immunoprecipitation assays. Furthermore, using the GSE160749 dataset from the Gene Expression Omnibus database, it was revealed that MYH9 protein expression was downregulated in AS samples. Subsequently, lentiviral vectors were constructed to induce overexpression of MYH9, which in turn reduced SSC apoptosis and counteracted the apoptosis triggered by Linc00893 knockdown. In conclusion, the present study identified the role of Linc00893 in AS, particularly its regulatory impact on sperm motility, SSC vitality and MYH9 expression. These findings may provide information on the potential regulatory mechanisms in AS development, and identify Linc00893 and MYH9 as possible targets for diagnosing and treating AS‑related disorders.
View Figures
View References

Related Articles

Journal Cover

February-2024
Volume 29 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Lu H, Xu D, Zhao L, Ruan H, Wang A, Hu J, Xiao M and Lu W: Exploring the regulatory role of Linc00893 in asthenozoospermia: Insights into sperm motility and SSC viability. Mol Med Rep 29: 20, 2024
APA
Lu, H., Xu, D., Zhao, L., Ruan, H., Wang, A., Hu, J. ... Lu, W. (2024). Exploring the regulatory role of Linc00893 in asthenozoospermia: Insights into sperm motility and SSC viability. Molecular Medicine Reports, 29, 20. https://doi.org/10.3892/mmr.2023.13143
MLA
Lu, H., Xu, D., Zhao, L., Ruan, H., Wang, A., Hu, J., Xiao, M., Lu, W."Exploring the regulatory role of Linc00893 in asthenozoospermia: Insights into sperm motility and SSC viability". Molecular Medicine Reports 29.2 (2024): 20.
Chicago
Lu, H., Xu, D., Zhao, L., Ruan, H., Wang, A., Hu, J., Xiao, M., Lu, W."Exploring the regulatory role of Linc00893 in asthenozoospermia: Insights into sperm motility and SSC viability". Molecular Medicine Reports 29, no. 2 (2024): 20. https://doi.org/10.3892/mmr.2023.13143