Osteopontin Regulates Endometrial Stromal Cell Migration in Endometriosis through the PI3K Pathway
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⤵ 19 in-corpus citations
Abstract
Endometriosis is generally characterized as a tumor-like disease because of its potential for distant metastasis and local tissue invasion, while whether osteopontin (OPN) plays a role in the pathogenesis of endometriosis has not been thoroughly investigated. We investigated the expression of OPN, urokinase plasminogen activator (uPA), phosphatidylinositol 3 kinase (PI3K), and phospho-PI3 kinase (p-PI3K) in endometrial stromal cells (ESCs). The serum concentration of OPN was determined by enzyme-linked immunosorbent assays (ELISA). OPN was downregulated to explore the corresponding change of uPA, p-PI3K, F-actin, and α-tubulin. The expression of OPN, uPA, PI3K, and p-PI3K was evaluated by western blot and quantitative real-time PCR (RT-qPCR) and the expression of F-actin and α-tubulin was confirmed by immunofluorescence assay. The proliferation and migration abilities of ESCs were investigated by CCK8, transwell, and wound scratch assays. Endometrial OPN, p-PI3K, and uPA expressions and serum OPN levels were increased in patients with endometriosis compared with the control. The expressions of p-PI3K, uPA, and α-tubulin were decreased by siRNA-OPN interference in ectopic ESCs. Activation and inhibition of the PI3K pathway apparently upregulate and downregulate uPA expression. Knockdown of OPN and inhibition of the PI3K pathway remarkably inhibited cell migration in ectopic ESCs. Meanwhile, activation of the PI3K pathway promoted the migration ability of ectopic ESCs. OPN may regulate the expression of uPA through the PI3K signal pathway to affect the migration ability of ESCs, indicating that OPN, uPA, and the PI3K pathway may be potential targets for interrupting development of endometriosis.
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Cited by (19)
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- Additional file 3 of TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis 2024
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- Additional file 2 of TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis 2024
- Research Progress in TCM for Intermenstrual Bleeding 2024
- Additional file 3 of TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis 2024
- Additional file 1 of TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis 2024
- Additional file 2 of TIM-3 regulates the proliferation by BDNF-mediated PI3K/AKT axis in the process of endometriosis 2024
- Moutan Cortex extract inhibited the proliferation and migration of endometrial stromal cells by inhibiting OPN-induced, MAPK-mediated MMP9 activation 2023
- Effects of Progestin on Modulation of the Expression of Biomarkers in Endometriosis 2023
- Osteopontin as a marker of endometriosis — the current state of knowledge 2023
- Research advances in endometriosis-related signaling pathways: A review 2023
- Omics-based novel strategies in the diagnosis of endometriosis 2023
- Osteopontin Splicing Isoforms Contribute to Endometriotic Proliferation, Migration, and Epithelial-Mesenchymal Transition in Endometrial Epithelial Cells 2022
- CHCHD2 Regulates Mitochondrial Function and Apoptosis of Ectopic Endometrial Stromal Cells in the Pathogenesis of Endometriosis 2022
- Circulating proteomic profiles associated with endometriosis in adolescents and young adults 2022
- LncRNA BANCR Promotes Endometrial Stromal Cell Proliferation and Invasion in Endometriosis via the miR-15a-5p/TRIM59 Axis 2022
- SMURF1-mediated ubiquitylation of SHP-1 promotes cell proliferation and invasion of endometrial stromal cells in endometriosis 2021
- TRIM65 Promotes Invasion of Endometrial Stromal Cells by Activating ERK1/2/C-myc Signaling via Ubiquitination of DUSP6 2020
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