The EMT signaling pathways in endometrial carcinoma
- PMID: 22911547
- DOI: 10.1007/s12094-012-0866-3
The EMT signaling pathways in endometrial carcinoma
Abstract
Endometrial cancer (EC) is the most common gynecologic malignancy of the female genital tract and the fourth most common neoplasia in women. In EC, myometrial invasion is considered one of the most important prognostic factors. For this process to occur, epithelial tumor cells need to undergo an epithelial to mesenchymal transition (EMT), either transiently or stably, and to differing degrees. This process has been extensively described in other types of cancer but has been poorly studied in EC. In this review, several features of EMT and the main molecular pathways responsible for triggering this process are investigated in relation to EC. The most common hallmarks of EMT have been found in EC, either at the level of E-cadherin loss or at the induction of its repressors, as well as other molecular alterations consistent with the mesenchymal phenotype-like L1CAM and BMI-1 up-regulation. Pathways including progesterone receptor, TGFβ, ETV5 and microRNAs are deeply related to the EMT process in EC.
Similar articles
-
MiR-195 inhibits migration, invasion and epithelial-mesenchymal transition (EMT) of endometrial carcinoma cells by targeting SOX4.J Biosci. 2019 Dec;44(6):146. J Biosci. 2019. PMID: 31894127
-
Regulation of epithelial-mesenchymal transition in endometrial cancer: connecting PI3K, estrogen signaling, and microRNAs.Clin Transl Oncol. 2016 Nov;18(11):1056-1061. doi: 10.1007/s12094-016-1492-2. Epub 2016 Feb 8. Clin Transl Oncol. 2016. PMID: 26856598 Review.
-
MicroRNA-106b modulates epithelial-mesenchymal transition by targeting TWIST1 in invasive endometrial cancer cell lines.Mol Carcinog. 2014 May;53(5):349-59. doi: 10.1002/mc.21983. Epub 2013 Sep 3. Mol Carcinog. 2014. PMID: 24002805
-
Epithelial-to-mesenchymal transition and stem cells in endometrial cancer.Hum Pathol. 2013 Oct;44(10):1973-81. doi: 10.1016/j.humpath.2013.04.009. Epub 2013 Jul 8. Hum Pathol. 2013. PMID: 23845467 Review.
-
MicroRNA-194 inhibits epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1.Mol Cancer. 2011 Aug 18;10:99. doi: 10.1186/1476-4598-10-99. Mol Cancer. 2011. PMID: 21851624 Free PMC article.
Cited by
-
Palmitic Acid Exerts Anti-Tumorigenic Activities by Modulating Cellular Stress and Lipid Droplet Formation in Endometrial Cancer.Biomolecules. 2024 May 20;14(5):601. doi: 10.3390/biom14050601. Biomolecules. 2024. PMID: 38786008 Free PMC article.
-
Genome-Wide Association Studies and Runs of Homozygosity to Identify Reproduction-Related Genes in Yorkshire Pig Population.Genes (Basel). 2023 Nov 27;14(12):2133. doi: 10.3390/genes14122133. Genes (Basel). 2023. PMID: 38136955 Free PMC article.
-
Targeting c-MYC: a potential non-hormonal therapeutic approach for endometriosis treatment.Front Cell Dev Biol. 2023 Nov 21;11:1225055. doi: 10.3389/fcell.2023.1225055. eCollection 2023. Front Cell Dev Biol. 2023. PMID: 38078012 Free PMC article.
-
Combined PI3K Inhibitor and Eribulin Enhances Anti-Tumor Activity in Preclinical Models of Paclitaxel-Resistant, PIK3CA-Mutated Endometrial Cancer.Cancers (Basel). 2023 Oct 8;15(19):4887. doi: 10.3390/cancers15194887. Cancers (Basel). 2023. PMID: 37835582 Free PMC article.
-
ETV5 transcriptionally activates TGFβ1 and promotes cancer cell invasion and migration of NSCLC.J Mol Histol. 2023 Oct;54(5):419-426. doi: 10.1007/s10735-023-10148-3. Epub 2023 Sep 1. J Mol Histol. 2023. PMID: 37656259
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials