TSPYL2 regulated by miR-301a-3p contributes to impaired decidualization in polycystic ovary syndrome
- 1Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550 Japan
- 2Nagoya University Institute for Advanced Research, Nagoya, Japan
- 3Department of Obstetrics and Gynecology, Aichi Medical University School of Medicine, Nagakute, Japan
Abstract
Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders associated with female infertility. Increasing evidence suggests that impaired endometrial receptivity, in addition to ovulatory dysfunction, may contribute to infertility in women with PCOS. However, the molecular mechanisms underlying defective decidualization in PCOS remain poorly understood. We observed impaired decidualization in both a prenatally androgenized mouse model and primary endometrial stromal cells from patients with PCOS. Testis-specific Y-encoded-like protein 2 (TSPYL2) displayed aberrant expression dynamics in PCOS, with elevated expression in the proliferative phase but insufficient induction during decidualization. Silencing TSPYL2 impaired decidualization and reduced implantation capacity in vitro and in vivo. Transcriptomic analysis further showed that TSPYL2 knockdown was associated with increased cell-cycle-associated signatures and reduced expression of hormone-responsive, decidualization- and endometrial receptivity-associated genes. Serum miR-301a-3p was upregulated during the secretory phase in PCOS and directly targeted the 3′ untranslated region of TSPYL2, suppressing its expression. Our findings suggest that elevated miR-301a-3p may impair decidualization by targeting TSPYL2, thereby contributing to defective endometrial function in PCOS.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1038/s41598-026-65152-w.
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BibTeX
@article{ruan2026tspyl2,
title = {{TSPYL2 regulated by miR-301a-3p contributes to impaired decidualization in polycystic ovary syndrome}},
author = {Jiali Ruan and Ayako Muraoka and Akira Yokoi and Bayasula and Kosuke Yoshida and Takehiko Takeda and Tomomi Seki and Natsuki Miyake and Reina Sonehara and Tomoko Nakamura and Satoko Osuka and Hiroaki Kajiyama},
journal = {Scientific Reports},
year = {2026},
month = aug,
doi = {10.1038/s41598-026-65152-w},
url = {https://doi.org/10.1038/s41598-026-65152-w},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - TSPYL2 regulated by miR-301a-3p contributes to impaired decidualization in polycystic ovary syndrome
AU - Jiali Ruan
AU - Ayako Muraoka
AU - Akira Yokoi
AU - Bayasula
AU - Kosuke Yoshida
AU - Takehiko Takeda
AU - Tomomi Seki
AU - Natsuki Miyake
AU - Reina Sonehara
AU - Tomoko Nakamura
AU - Satoko Osuka
AU - Hiroaki Kajiyama
PY - 2026
DA - 2026/08/05
JO - Scientific Reports
DO - 10.1038/s41598-026-65152-w
UR - https://doi.org/10.1038/s41598-026-65152-w
AB - Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders associated with female infertility. Increasing evidence suggests that impaired endometrial receptivity, in addition to ovulatory dysfunction, may contribute to infertility in women with PCOS. However, the molecular mechanisms underlying defective decidualization in PCOS remain poorly understood. We observed impaired decidualization in both a prenatally androgenized mouse model and primary endometrial stromal cells from patients with PCOS. Testis-specific Y-encoded-like protein 2 (TSPYL2) displayed aberrant expression dynamics in PCOS, with elevated expression in the proliferative phase but insufficient induction during decidualization. Silencing TSPYL2 impaired decidualization and reduced implantation capacity in vitro and in vivo. Transcriptomic analysis further showed that TSPYL2 knockdown was associated with increased cell-cycle-associated signatures and reduced expression of hormone-responsive, decidualization- and endometrial receptivity-associated genes. Serum miR-301a-3p was upregulated during the secretory phase in PCOS and directly targeted the 3′ untranslated region of TSPYL2, suppressing its expression. Our findings suggest that elevated miR-301a-3p may impair decidualization by targeting TSPYL2, thereby contributing to defective endometrial function in PCOS. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1038/s41598-026-65152-w.
SN - 2045-2322
ER -