Abstract
Aim: Azoospermia accounts for 10–20% of male infertility. In 20–30% of affected males, genetic abnormalities are the leading cause of azoospermia. LncRNAs can regulate spermatogenic cell development. Methods: This study chose 76 azoospermia patients and 36 healthy males. The gene expression was examined using the qRT-PCR technique. Results: IGSF11-AS1 and BVES-AS appeared to be considerably underexpressed in the patients; however, only IGSF11-AS1 demonstrated a significant biomarker role. Additionally, IGSF11-AS1 expression was positively correlated with testosterone but was negatively correlated with follicle-stimulating hormone (FSH) and luteinizing hormone (LH). For the BVES-AS gene, however, FSH and LH had a negative correlation. Conclusion: As a result of its low expression level in tissue samples, IGSF11-AS1 has a biomarker role for early azoospermia detection.
Infertility affects 8–12% of childbearing-age couples, with around 50% of total cases of male infertility, while azoospermia, or the absence of sperm, accounts for 15% of cases.
In 20–30% of affected males, genetic abnormalities may be the leading cause of azoospermia. However, the molecular mechanisms related to spermatogenic failure are poorly understood.
Due to the widespread expression of lncRNAs in the testis, these molecules may be biomarkers for abnormalities affecting the male reproductive system.
Expression levels of IGSF11-AS1 and BVES-AS were considerably lower in infertile patients than in fertile controls.
IGSF11-AS1 can be a potential biomarker for azoospermia detection with AUCs of 0.84.
Infertile patients had significantly greater LH and FSH levels. However, testosterone levels were considerably reduced in patients compared with control males.
IGSF11-AS1 expression level showed a negative association with LH and FSH hormones, with a positive correlation for testosterone.
The BVES-AS gene has negatively correlated with the LH and FSH expression levels, with no correlation shown for testosterone.
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Acknowledgments
The authors thank the patients who participated in this project.
Author contributions
Conceptualization: MIIJ, NJKM, RS. Data curation: MIIJ, NJKM, AHSS. Formal analysis: MIIJ, AHSS, RS. Methodology: MIIJ, NJKM, RS. Visualization: MIIJ, RS. Writing-original draft: MIIJ, NJKM, RS. Writing-review and editing: MIIJ, AHSS, RS.
Financial disclosure
The authors have no financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Competing interests disclosure
The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, stock ownership or options and expert testimony.
Writing disclosure
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
The authors state that they have obtained appropriate institutional review board approval (no. 52/422368/1) and/or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations.
In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.