Published online Dec 16, 2021. doi: 10.12998/wjcc.v9.i35.11036
Peer-review started: July 1, 2021
First decision: July 26, 2021
Revised: July 27, 2021
Accepted: October 27, 2021
Article in press: October 27, 2021
Published online: December 16, 2021
Processing time: 161 Days and 21 Hours
Androgen insensitivity syndrome is an X-linked recessive genetic disease caused by mutations in the androgen receptor gene (AR). However, the underlying molecular mechanisms for the majority of AR variants remain unclear. In this study, we identified a point variant in three patients with complete androgen insensitivity syndrome (CAIS), summarized the correlation analysis, and performed a literature review.
The proband was raised as a girl. In infancy, she was first referred to hospital with a right inguinal hernia. Ultrasonography revealed the absence of a uterus and ovaries, and a testis-like structure located at the inguinal canal. Further diagnostic workup detected a 46, XY karyotype, and fluorescence in situ hybridization analysis showed the presence of the SRY gene. Histological analysis revealed the excised tissue to be testicular. Twelve years later, she was admitted to our hospital with a lack of breast development. Her pubic hair and breasts were Tanner stage I. She had normal female external genitalia. Blood hormone tests showed normal testosterone levels, low estradiol levels, and high gonadotropin levels. Her two siblings underwent similar examinations, and all three had a rare hemizygous missense mutation in AR: c.2678C>T. In vitro functional analyses revealed decreased nuclear translocation in AR-c.2678C>T mutation cells.
This case of CAIS was caused by an AR variant (c.2678C>T). Functional studies showed impaired nuclear translocation ability of the mutant protein.
Core Tip: A hemizygous variant c.2678C>T (p.P893L) was found in the Ligand-binding domain of the AR gene in a Chinese family affected with complete androgen insensitivity syndrome (CAIS). Online prediction tools were used to predict the disease-causing potential of this variant. Structural analysis revealed that the amino acid substitution affected protein properties, and in vitro functional studies showed the nuclear translocation ability of the mutant protein to be impaired. CAIS in this family was concluded to be caused by the c.2678C>T variant, whose pathogenesis resulting in an androgen insensitivity syndrome phenotype may be related to decreased nuclear translocation.