New insights of epithelial-mesenchymal transition in cancer metastasis.
نویسندگان
چکیده
Epithelial-mesenchymal transition (EMT) is a key step during embryonic morphogenesis, heart development, chronic degenerative fibrosis, and cancer metastasis. Several distinct traits have been conveyed by EMT, including cell motility, invasiveness, resistance to apoptosis, and some properties of stem cells. Many signal pathways have contributed to the induction of EMT, such as transforming growth factor-beta, Wnt, Hedgehog, Notch, and nuclear factor-kappaB. Over the last few years, increasing evidence has shown that EMT plays an essential role in tumor progression and metastasis. Understanding the molecular mechanism of EMT has a great effect in unraveling the metastatic cascade and may lead to novel interventions for metastatic disease.
منابع مشابه
Analysis of epithelial mesenchymal transition markers in breast cancer cells in response to stromal cell-derived factor 1
Introduction: Metastasis is the main cause of cancer death; however, the underlying mechanisms of metastasis are largely unknown. The chemokine of stromal cell-derived factor 1 (SDF1) and the process of epithelial mesenchymal transition (EMT), both have been declared as important factors to promote cancer metastasis; however, Conspicuously, the relation between them has not been recognized well...
متن کاملEpithelial to mesenchymal transition concept in Cancer: Review article
Owing to this fact that most of the mortalities in cancers are as a result of metastasis, study on the involved pathways in metastasis including Epithelial to mesenchymal transition (EMT) would be so critical and important. Up to date, several extensive studies have been carried out to determine the correlation between EMT and cancer and their results have shown that the EMT plays pivotal role ...
متن کاملMesenchymal Stem Cells Trigger Epithelial to Mesenchymal Transition in the HT-29 Colorectal Cancer Cell Line
Background and Objective: Mesenchymal stem cells (MSCs) promote metastasis in colorectal cancer; however, the mechanism underlying this process is not fully understood. Epithelial to mesenchymal transition (EMT) is a key step in tumor acquisition of metastatic phenotype. We aimed to investigate the effect of MSCs on the expression of EMT markers, as well as cancer stem cell markers in HT-29 col...
متن کاملCrosstalk between Tumor Cells and Immune System Leads to Epithelial-Mesenchymal Transition Induction and Breast Cancer Progression
Herein, we review the current findings of how a variety of accessory cells could participate in shaping the tumor microenvironment and supporting the mechanisms by which cancer cells undertake the epithelial-mesenchymal transition (EMT). EMT, a complex of phenotypic changes, promotes cancer cell invasion and creates resistance to chemotherapies. Among the accessory cells present in the EMT, imm...
متن کاملNDRG2 Regulates the Expression of Genes Involved in Epithelial Mesenchymal Transition of Prostate Cancer Cells
Background: Metastasis is the main cause of prostate cancer (PCa) death. The inhibitory effect of N-myc downstream-regulated gene 2 (NDRG2) on the invasiveness properties of PCa cells has been demonstrated previously. However, its underlying mechanisms have not yet been investigated. The present study aimed to investigate the effects of NDRG2 overexpression on the expression of genes involved i...
متن کاملEpithelial-mesenchymal transition in breast cancer progression and metastasis
Breast cancer is the most common cancer in women, and approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells. Epithelial-mesenchymal transition (EMT) is a vital process for large-scale cell movement during morphogenesis at the time of embryonic development. Tumor cells usurp this developmental program to execute the multi-step process of tum...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Acta biochimica et biophysica Sinica
دوره 40 7 شماره
صفحات -
تاریخ انتشار 2008