フルテキストURL
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著者
Vu, Thuy Ha Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
Nakamura, Keiichiro Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine Kaken ID publons researchmap
Shigeyasu, Kunitoshi Department of Gastroenterological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
Kashino, Chiaki Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
Okamoto, Kazuhiro Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
Kubo, Kotaro Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
Kamada, Yasuhiko Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine ORCID Kaken ID publons researchmap
Masuyama, Hisashi Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine Kaken ID publons researchmap
抄録
This study investigated the correlation of Apolipoprotein-B mRNA-editing complex 3B (APOBEC3B) expression with hypoxia inducible factor 1α (HIF-1α), Kirsten rat sarcoma virus (KRAS) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) in endometriosis patients, and the inhibitory effects of APOBEC3B knockdown in a human endometriotic cell line. Here, APOBEC3B, HIF-1α, KRAS, and PIK3CA were examined in patients with and without endometriosis using reverse transcription polymerase chain reaction (RT-PCR). The apoptosis, cell proliferation, invasion, migration, and biological function of APOBEC3B knockdown were explored in 12Z immortalized human endometriotic cell line. We observed APOBEC3B, HIF-1α, KRAS and PIK3CA expressions were significantly higher in endometriosis patients (p < 0.001, p < 0.001, p = 0.029, p = 0.001). Knockdown of APOBEC3B increased apoptosis, which was 28.03% and 22.27% higher than in mock and control siRNA samples, respectively. APOBEC3B knockdown also decreased PIK3CA expression and increased Caspase 8 expression, suggesting a potential role in the regulation of apoptosis. Furthermore, knockdown of APOBEC3B significantly inhibited cell proliferation, invasion, and migration compared to mock and control siRNA. (Cell proliferation: mock: p < 0.001 and control siRNA: p = 0.049. Cell invasion: mock: p < 0.001 and control siRNA: p = 0.029. Cell migration: mock: p = 0.004, and control siRNA: p = 0.014). In conclusion, this study suggests that APOBEC3B may be a new potential therapeutic target for endometriosis.
キーワード
Apolipoprotein-B mRNA-editing complex 3B
Endometriosis
Apoptosis
Potential therapeutic target
備考
The version of record of this article, first published in Scientific Reports, is available online at Publisher’s website: http://dx.doi.org/10.1038/s41598-024-76589-2
発行日
2024-10-23
出版物タイトル
Scientific Reports
14巻
1号
出版者
Nature Portfolio
開始ページ
24968
ISSN
2045-2322
資料タイプ
学術雑誌論文
言語
英語
OAI-PMH Set
岡山大学
論文のバージョン
publisher
PubMed ID
DOI
Web of Science KeyUT
ライセンス
http://creativecommons.org/licenses/by-nc-nd/4.0/
Citation
Vu, T.H., Nakamura, K., Shigeyasu, K. et al. Apolipoprotein-B mRNA-editing complex 3B could be a new potential therapeutic target in endometriosis. Sci Rep 14, 24968 (2024). https://doi.org/10.1038/s41598-024-76589-2
助成機関名
Japan Society for the Promotion of Science
助成番号
22K09619
23K15815