ArticleCell death and differentiation2023
Deficiency of cancer/testis antigen gene CT55 causes male infertility in humans and mice.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Heterogeneity in cancer: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Genetic and epigenetic insights into non-obstructive azoospermia: mechanisms, biomarkers, and clinical perspectives.Reproductive biology and endocrinology : RB&E · 2025Review
- Selenium-Enriched Aspergillus oryzae A02 Enhances Testicular Antioxidant Capacity in Mice by Regulating Intestinal Microbiota and Serum Metabolite.Biological trace element research · 2025Article
- Interplay of Ferroptosis, Cuproptosis, Autophagy and Pyroptosis in Male Infertility: Molecular Crossroads and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Autophagy accompanying the developmental process of male germline stem cells.Cell and tissue research · 2024Review
- Spem2, a novel testis-enriched gene, is required for spermiogenesis and fertilization in mice.Cellular and molecular life sciences : CMLS · 2024Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Cancer/Testis Antigen (CTA) genes comprise a group of genes whose expression under physiological conditions is restricted to the testis but is activated in many human cancers. Depending on the particular expression pattern, the CTA genes are speculated to play a role in spermatogenesis, but evidence is limited thus far. Here, we reported patients with a hemizygous nonsense mutation in cancer-testis antigen 55 (CT55) suffering from male infertility with extreme disruption in sperm production, morphology, and locomotion. Specifically, the insufficiency of sperm individualization, excessive residue of unnecessary cytoplasm, and defects in acrosome development were evident in the spermatozoa of the patients. Furthermore, mouse models with depletion of Ct55 showed accelerated infertility with age, mimicking the defects in sperm individualization, unnecessary cytoplasm removal, and meanwhile exhibiting the disrupted cumulus-oocyte complex penetration. Mechanistically, our functional experiments uncovered CT55 as a new autophagic manipulator to regulate spermatogenesis via selectively interacting with LAMP2 and GABARAP (which are key regulators in the autophagy process) and further fine-tuning their expression. Therefore, our findings revealed CT55 as a novel CTA gene involved in spermatogenesis due to its unprecedented autophagy activity.
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