Purpose: To explore the exact mechanism through which emodin down-regulates the migration and invasion abilities of endometrial stromal cells. Moreover, to explore the theoretical basis of emodin in the treatment of endometriosis.
Patients And Methods: Endometriosis endometrial stromal cells (EESs) were cultured from 15 women with endometriosis and control endometrial stromal cells (CESs) were cultured from 12 women without endometriosis. The levels of proteins were evaluated by Western blot. The migration and invasion abilities of cells were detected by transwell assays.
Results: The abilities of migration and invasion of EESs were much stronger than those of CESs. After treated with emodin, the migration and invasion abilities of EESs and CESs were significantly down-regulated, and the levels of integrin-linked kinase (ILK) and p-GSK-3β were statistically down-regulated in EESs. Besides that, the expression of keratin was up-regulated while the expression of vimentin, β-catenin and slug were all down-regulated by emodin in a dose- and time-dependent manner. Silencing of ILK gene in EESs also achieved the above effects, which were strengthened by emodin. Conversely, exogenous expression of ILK in CESs increased the expression of p-GSK-3β, which were abrogated by emodin. Furthermore, SB216763 increased migration and invasion abilities of CESs by facilitating the epithelial-mesenchymal transition (EMT) through up-regulating levels of p-GSK-3β, β-catenin and slug, which were also abrogated by emodin.
Conclusion: Emodin inhibits the migration and invasion abilities of human endometrial stromal cells by reversing the EMT via ILK/GSK-3β pathway. So, emodin may be considered as a promising targeted therapy for endometriosis.
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http://dx.doi.org/10.2147/DDDT.S262816 | DOI Listing |
Afr J Reprod Health
November 2024
Department of Obstetrics and Gynecology, Wuxi No.2 People's Hospital, Wuxi 214002, Jiangsu Province, China.
Cervical cancer (CC) is a malignant tumor in females characterized by high incidence and mortality rates, often resulting in a poor prognosis for patients. Zoledronic acid (ZA), a third-generation bisphosphonate, exhibits anti-tumor properties across various types of tumors. To further understand the effect of ZA in the treatment of CC, this article included two kinds of human CC cells (CCCs) as the research object, examining the impact of varying levels of ZA on the cells' biological properties.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of General Surgery, Tianjin First Center Hospital, Tianji, 300384, China.
A number of various human malignancies have been associated with abnormal microRNAs (miRNA) expression. There are evidence that miR-200 operates as both tumor suppressor and an onco-miR in a variety of tumors. In this study, we evaluated the effects of miR-200 on the proliferation and migration of pancreatic cancer cells, as well as the underlying molecular pathways.
View Article and Find Full Text PDFJ Bioenerg Biomembr
January 2025
Department of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China.
To investigate the role of silent information regulator 6 (SIRT6) in regulating podocyte injury in diabetic nephropathy (DN) through autophagy mediated by Notch signaling pathway. A blank control group (group A), a diabetic nephropathy group (group B), and a Sirt6 intervention group (group C) were established. The group A cells were human normal glomerular podocyte cell lines (HGPCs) without any treatment.
View Article and Find Full Text PDFCancer Cell Int
January 2025
Department of Otolaryngology, Pudong Gongli Hospital, Shanghai, 200135, China.
Background: Specific molecular mechanisms by which AURKA promoted LSCC metastasis were still unknown.
Methods: Bioinformatic analysis was performed the relationship between TRIM28 and LSCC. Immunohistochemistry, Co-IP assay, Rt-PCR and Western Blot were used to examine the expression of related molecular.
Chin Med
January 2025
Department of Clinical Chinese Pharmacy, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 102488, China.
Background: With extended gefitinib treatment, the therapeutic effect in some non-small cell lung cancer (NSCLC) patients declined with the development of drug resistance. Aidi injection (ADI) is utilized in various cancers as a traditional Chinese medicine prescription. This study explores the molecular mechanism by which ADI, when combined with gefitinib, attenuates gefitinib resistance in PC9GR NSCLC cells.
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