Gynecologic and obstetric investigation · 2026
SEMA3C Promotes the Progression of Endometriosis by Inducing Ferroptosis and Enhancing the Viability and Migration of Endometrial Stromal Cells.
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Li Yan, Zhang Yi
Аннотация
OBJECTIVES: The aim of this study was to examine SEMA3C expression in endometriosis (EMs) and its relationship with ferroptosis in human endometrial stromal cells (HESCs).
DESIGN: This experimental study used patient tissue samples and in vitro gain- and loss-of-function assays. Participants/Materials: The participants and materials involved endometrial tissues from 30 patients with EMs and 30 controls, including paired ectopic and eutopic tissues from 10 patients, and primary HESCs.
SETTING: This study was set in the Affiliated Women and Children's Hospital of Ningbo University and its associated laboratory facilities.
METHODS: SEMA3C expression was assessed by immunohistochemistry, Western blotting, and qRT-PCR in this study. Primary HESCs were subjected to SEMA3C overexpression or siRNA-mediated knockdown. Cell viability, migration, iron content, lipid peroxidation, antioxidant activity, inflammatory cytokines, and ferroptosis regulators were analyzed. Ferrostatin-1 was used for rescue experiments.
RESULTS: This experimental study showed that SEMA3C was upregulated in ectopic tissues versus controls (p < 0.001) and correlated with disease severity (stages III-IV vs. I-II, p < 0.01). Ectopic lesions showed higher SEMA3C mRNA than matched eutopic endometrium (p < 0.001). Ectopic tissues and SEMA3C-overexpressing HESCs showed increased ferroptosis-related oxidative and inflammatory changes. SEMA3C overexpression enhanced HESC viability and migration, increased ACSL4, and decreased Nrf2, GPX4, and SLC7A11 expression (p < 0.001). SEMA3C knockdown or Ferrostatin-1 attenuated these alterations and suppressed HESC viability and migration (p < 0.01).
LIMITATIONS: The findings of this study are based on clinical tissues and in vitro HESC experiments, and in vivo validation and prospective confirmation are required.
CONCLUSIONS: It was shown thatSEMA3C promotes HESC viability and migration through ferroptosis-related oxidative and inflammatory mechanisms, identifying the SEMA3C-ferroptosis axis as a potential pathogenic pathway in EMs.
DESIGN: This experimental study used patient tissue samples and in vitro gain- and loss-of-function assays. Participants/Materials: The participants and materials involved endometrial tissues from 30 patients with EMs and 30 controls, including paired ectopic and eutopic tissues from 10 patients, and primary HESCs.
SETTING: This study was set in the Affiliated Women and Children's Hospital of Ningbo University and its associated laboratory facilities.
METHODS: SEMA3C expression was assessed by immunohistochemistry, Western blotting, and qRT-PCR in this study. Primary HESCs were subjected to SEMA3C overexpression or siRNA-mediated knockdown. Cell viability, migration, iron content, lipid peroxidation, antioxidant activity, inflammatory cytokines, and ferroptosis regulators were analyzed. Ferrostatin-1 was used for rescue experiments.
RESULTS: This experimental study showed that SEMA3C was upregulated in ectopic tissues versus controls (p < 0.001) and correlated with disease severity (stages III-IV vs. I-II, p < 0.01). Ectopic lesions showed higher SEMA3C mRNA than matched eutopic endometrium (p < 0.001). Ectopic tissues and SEMA3C-overexpressing HESCs showed increased ferroptosis-related oxidative and inflammatory changes. SEMA3C overexpression enhanced HESC viability and migration, increased ACSL4, and decreased Nrf2, GPX4, and SLC7A11 expression (p < 0.001). SEMA3C knockdown or Ferrostatin-1 attenuated these alterations and suppressed HESC viability and migration (p < 0.01).
LIMITATIONS: The findings of this study are based on clinical tissues and in vitro HESC experiments, and in vivo validation and prospective confirmation are required.
CONCLUSIONS: It was shown thatSEMA3C promotes HESC viability and migration through ferroptosis-related oxidative and inflammatory mechanisms, identifying the SEMA3C-ferroptosis axis as a potential pathogenic pathway in EMs.