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Showing 1–45 of 45 results
  • Epithelial–mesenchymal transition (EMT) is crucial in embryogenesis and can be exploited by cancer cells to gain metastatic abilities. A hallmark of EMT is E-cadherin loss. In 2000, Snail was reported as the first E-cadherin repressor identified in the context of EMT, advancing our understanding of embryonic development and cancer progression.

    • Yutong Sun
    • Li Ma
    News & Views
    Nature Cell Biology
    Volume: 26, P: 29-30
  • Blanpain and colleagues provide evidence that the small RHO GTPase, RHOJ, mediates resistance to chemotherapy in tumour cells that have undergone epithelial-to-mesenchymal transition by enabling these cells to tolerate replicative stress and promote DNA damage repair.

    • Anna Dart
    Research Highlights
    Nature Reviews Cancer
    Volume: 23, P: 349
  • ZEB1-mediated epithelial-mesenchymal transition (EMT) and cellular plasticity promotes metastasis in pancreatic cancer.

    • Anna Dart
    Research Highlights
    Nature Reviews Cancer
    Volume: 17, P: 373
    • Sarah Seton-Rogers
    Research Highlights
    Nature Reviews Cancer
    Volume: 16, P: 617
  • BMI1, a gene expressed in stem cells, is involved in EMT and is a target of the transcription factor TWIST1.

    • Nicola McCarthy
    Research Highlights
    Nature Reviews Cancer
    Volume: 10, P: 667
  • TGFβ signalling induces EMT and elicits apoptosis by switching SOX4 from acting as a tumour promoter to a tumour suppressor.

    • Paulina Strzyz
    Research Highlights
    Nature Reviews Molecular Cell Biology
    Volume: 17, P: 202-203
  • Neural crest cells switch from expressing E-cadherin to expressing N-cadherin to undergo contact inhibition of locomotion.

    • Katharine H. Wrighton
    Research Highlights
    Nature Reviews Molecular Cell Biology
    Volume: 16, P: 518
  • Fatty acid oxidation and increased acetyl-CoA levels act to suppress endothelial–mesenchymal transition.

    • Paulina Strzyz
    Research Highlights
    Nature Reviews Molecular Cell Biology
    Volume: 19, P: 211
  • D’Amico et al. show that, in the presence of oncogenic RAS mutations, STAT3 acts as a tumour modifier by regulating the epithelial differentiation of pancreatic and lung cancer cells via p63.

    • Maria Giuseppina Baratta
    Research Highlights
    Nature Reviews Cancer
    Volume: 18, P: 664-665
  • Two papers providein vivoevidence for plasticity of epithelial and mesenchymal transitions, showing that EMT reversion is required for metastatic outgrowth.

    • Gemma K. Alderton
    Research Highlights
    Nature Reviews Cancer
    Volume: 13, P: 3
  • Cancer stem cells might arise by the epithelial-to-mesenchymal transition.

    • Xin-Hua Feng
    Research Highlights
    Nature Reviews Molecular Cell Biology
    Volume: 11, P: 466
  • A new study characterizes the epithelial versus mesenchymal properties of circulating tumour cells and identifies an interesting plasticity.

    • Darren J. Burgess
    Research Highlights
    Nature Reviews Cancer
    Volume: 13, P: 149
  • How does ZEB1 regulate self-renewal and migration?

    • Nicola McCarthy
    Research Highlights
    Nature Reviews Cancer
    Volume: 10, P: 6-7
  • Two recent papers have shown that EMT can be driven by both alternative splicing and chromatin modification.

    • Sarah Seton-Rogers
    Research Highlights
    Nature Reviews Cancer
    Volume: 11, P: 689
  • Two papers published inCellexpand our knowledge and raise new questions about how metastasis occurs in pancreatic cancer.

    • Sarah Seton-Rogers
    Research Highlights
    Nature Reviews Cancer
    Volume: 12, P: 151
  • Timothy Thomson and colleagues have used prostate and bladder cancer models, derived from human cell lines, to show that epithelial-to-mesenchymal transition can suppress tumour-initiating potential and colonization of distant organs.

    • Sarah Seton-Rogers
    Research Highlights
    Nature Reviews Cancer
    Volume: 12, P: 378-379
  • Two papers indicate the importance of TAZ in cancer biology.

    • Mhairi Skinner
    Research Highlights
    Nature Reviews Cancer
    Volume: 12, P: 82-83
  • Two studies published inNaturereport that epithelial–mesenchymal transition (EMT) is not required for metastasis in mouse tumour models of breast and pancreatic cancer; however, EMT can contribute to resistance to chemotherapy.

    • Sarah Seton-Rogers
    Research Highlights
    Nature Reviews Cancer
    Volume: 16, P: 1
  • Bracken and Goodall discuss why epithelial–mesenchymal transition (EMT) has so many regulators, but also consider whether many of these may be ‘false positives’.

    • Cameron P. Bracken
    • Gregory J. Goodall
    Comments & Opinion
    Nature Reviews Molecular Cell Biology
    Volume: 23, P: 89-90
  • Epithelial–mesenchymal transition (EMT) is crucial for development, and for dissemination and invasion of cancer cells. A study now identifies the apical–basolateral polarity status of epithelia as a checkpoint for EMT induction and tumour metastasis through aPKC–Par3-regulated degradation of the EMT transcription factor SNAI1.

    • Oana-Diana Persa
    • Carien M. Niessen
    News & Views
    Nature Cell Biology
    Volume: 21, P: 299-300
  • The roles of transforming growth factor β (TGF-β) depend on the cellular context. Paraspeckle component 1 now arises as a driver of epithelial-to-mesenchymal transition and stemness transcription factors to redirect effectors from tumour suppressive to pro-metastatic gene promoters, emerging as a contextual determinant of TGF-β function.

    • Fernando Salvador
    • Roger R. Gomis
    News & Views
    Nature Cell Biology
    Volume: 20, P: 367-369
  • With the emergence of increasingly potent androgen deprivation therapy, rates of treatment-emergent small-cell neuroendocrine prostate cancer are increasing. In a recent prospective study, Aggarwal and colleagues defined the frequency and clinical and genomic characteristics of these tumours.

    • Magdalena M. Grabowska
    • Robert J. Matusik
    News & Views
    Nature Reviews Urology
    Volume: 15, P: 662-663
  • Although the importance of epithelial to mesenchymal transition (EMT) is acknowledged in tumor metastasis, the contribution of the reverse process—MET—to cancer progression has been unclear. A new study shows that the miR-200 family regulates MET and metastatic colonization in breast cancer, suggesting that flexible transitions between EMT and MET, or epithelial-mesenchymal plasticity, may be crucial at different stages of metastasis (pages 1101–1108).

    • E W Thompson
    • I Haviv
    News & Views
    Nature Medicine
    Volume: 17, P: 1048-1049
  • The role of the epithelial-to-mesenchymal transition in tumour progression remains a topic of intense debate. Now, data on the role of Zeb1 in the metastatic spread of pancreatic cancer clarify apparently conflicting views by revealing context-specific, differential use of individual epithelial-to-mesenchymal transition transcription factors in cancer cell dissemination.

    • M. Angela Nieto
    News & Views
    Nature Cell Biology
    Volume: 19, P: 416-418
  • Epithelial to mesenchymal transition (EMT) is a fundamental process in both development and cancer progression. The transcription factor Elf5 is now reported as an upstream regulator of the key EMT inducer Snail2, and is shown to regulate the earliest known rewiring events required for tumour cell invasiveness and metastasis.

    • Haritha Mathsyaraja
    • Michael C. Ostrowski
    News & Views
    Nature Cell Biology
    Volume: 14, P: 1122-1123
  • The epithelial–mesenchymal transition (EMT) occurs in pre-metastatic cancer cells and is also associated with the acquisition of stem-cell-like characteristics. A molecular link between EMT and stemness now emerges with the finding that Bmi1, a polycomb protein that promotes self-renewal of certain stem-cell populations, is a direct transcriptional target of the EMT inducer, Twist1.

    • Alberto Martin
    • Amparo Cano
    News & Views
    Nature Cell Biology
    Volume: 12, P: 924-925
  • The microRNA miR-9 is induced by Myc in breast cancer cells where it targets the major epithelial adherens junction protein, E-cadherin. This primes the cancer cells for epithelial–mesenchymal transition (EMT) and also stimulates angiogenesis in tumours.

    • Yeesim Khew-Goodall
    • Gregory J. Goodall
    News & Views
    Nature Cell Biology
    Volume: 12, P: 209-211
  • The transcription factor Twist1 is overexpressed in tumours and can induce the epithelial–mesenchymal transition, resulting in increased invasiveness. Twist1 is now shown to regulate cancer cell migration and invasion in three-dimensional environments by activating the RAC1 GTPase through suppression of a let-7 microRNA family member.

    • Geoffrey Childs
    • Jeffrey E. Segall
    News & Views
    Nature Cell Biology
    Volume: 14, P: 337-339