Purpose: Epithelial-mesenchymal transition (EMT) endows cells with migratory and invasive properties, a prerequisite for the establishment of endometriotic lesions. However, the role EMT might play in the pathophysiology of endometriosis is still unknown. Therefore, we examined five recognized markers for EMT in endometrium and endometriosis: E-cadherin, N-cadherin, Twist, Snail and Slug.
Methods: Immunohistochemistry was used for peritoneal, ovarian and rectovaginal endometriotic lesions (n = 27) and endometrium (n = 13). Reverse transcription polymerase chain reaction was applied to tissue samples and primary cell cultures of endometriotic lesions (n = 9) and endometrium (n = 8).
Results: In endometriosis and endometrium E-cadherin, N-cadherin, Twist, Snail and Slug were expressed on protein and mRNA level. E-cadherin expression was strong in epithelial cells, but single E-cadherin-negative cells were frequently present in endometriosis. In endometriosis N-cadherin, Twist and Snail expression were upregulated in comparison with endometrium. The expression of E- and N-cadherin was inversely correlated, while that of N-cadherin and Twist was positively correlated.
Conclusion: This study strongly suggests that EMT may be regulated differently in endometriosis and the endometrium. Future research should further elucidate the regulation of EMT in the endometrium and endometriosis.
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http://dx.doi.org/10.1007/s00404-013-3040-4 | DOI Listing |
Eur J Dent
December 2024
School of Dentistry, University of Birmingham, Birmingham, United Kingdom.
Objectives: Epithelial-mesenchymal transition (EMT) is a process that shifts cellular phenotype. It is linked to several different inflammatory diseases including periodontitis. This study was conducted to investigate the involvement of the EMT process in an experimental periodontitis (EP) model.
View Article and Find Full Text PDFHua Xi Kou Qiang Yi Xue Za Zhi
December 2024
Institute of Stomatology, Binzhou Medical University, Yantai 264000, China.
Objectives: This study aimed to investigate the effects of silencing Ras homolog family member C (RhoC) on the proliferation, apoptosis, invasion, migration, and epithelial-mesenchymal transition (EMT) of salivary adenoid cystic carcinoma (SACC) and its molecular mechanisms.
Methods: A total of 27 SACC lesions and normal salivary gland tissues that were surgically resected at Qingdao Municipal Hospital from January 1, 2019 to March 1, 2024 were selected, and the expression levels of RhoC were detected by Western blot and immunohistochemistry. Three small interfering RNA (siRNAs) were designed to target the RhoC gene sequence, transfected into SACC-LM and SACC-83 cell lines, and evaluated for transfection efficiency.
Mol Cell Biochem
November 2024
Kindai University Faculty of Pharmacy, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Oxaliplatin (L-OHP) and 5-fluorouracil (5-FU) are used to treat colon cancer; however, resistance contributes to poor prognosis. Epithelial-mesenchymal transition (EMT) has been induced in tumor tissues after administration of anticancer drugs and may be involved in drug resistance. We investigated the mechanism of EMT induction in colon cancer cells treated with 5-FU and L-OHP.
View Article and Find Full Text PDFPathol Res Pract
December 2024
Clinical College of TCM, Hubei University of Traditional Chinese Medicine, Wuhan 430050, China.
Background: Epithelial-mesenchymal transition (EMT) is an essential process for the metastasis of multiple malignancies, including hepatocellular carcinoma (HCC). Farrerol is a plant-derived flavonoid and has significant pharmacological effects. However, the anticancer activities of farrerol have not been fully elucidated.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
October 2024
Department of Infectious Diseases, First Affiliated Hospital of Bengbu Medical University, Bengbu 233000, China.
Objective: To explore whether Yes-associated protein (YAP) affects occurrence and progression of liver fibrosis by regulating epithelial-mesenchymal transition (EMT).
Methods: In a 8-week-old C57BL/6 mouse model of CCl-induced liver fibrosis, the effect of verteporfin (a YAP inhibitor) intervention was assessed with HE staining and by detecting liver biochemistry and expressions of YAP and EMT-related genes using immunohistochemistry and Western blotting. Transcriptome and proteomic sequencing and informatics analysis were used to investigate the main downstream pathways of YAP in liver fibrosis.
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