Guidelines and definitions for research on epithelial–mesenchymal transition

Yang, Jing; Antin, Parker B.; Berx, Geert; Blanpain, Cédric; Brabletz, Thomas; Bronner, Marianne E.; Campbell, Kyra; Cano, Amparo; Casanova, Jordi; Christofori, Gerhard; Dedhar, Shoukat; Derynck, Rik; Ford, Heide L.; Fuxe, Jonas; Herreros, Antonio Garcı́a de; Goodall, Gregory J.; Hadjantonakis, Anna Katerina; Huang, Ruby Yun‐Ju; Kalcheim, Chaya; Kalluri, Raghu; Kang, Yibin; Khew‐Goodall, Yeesim; Levine, Herbert; Liu, Jinsong; Longmore, Gregory D.; Mani, Sendurai A.; Massagué, Joan; Mayor, Roberto; McClay, David R.; Mostov, Keith E.; Newgreen, Donald F.; Nieto, M. Ángela; Puisieux, Alain; Runyan, Raymond B.; Savagner, Pierre; Stanger, Ben Z.; Stemmler, Marc P.; Takahashi, Yoshiko; Takeichi, Masatoshi; Théveneau, Eric; Thiery, Jean Paul; Thompson, Erik W.; Weinberg, Robert A.; Williams, Elizabeth D.; Xing, Jianhua; Zhou, Binhua P.; Sheng, Guojun

doi:10.1038/s41580-020-0237-9

Cited by 1,257 publications

(1,125 citation statements)

References 92 publications

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“…Moreover, we detected the expression of EMT-related proteins in tumors derived from control or PNN-depleted xenografts, similar results were observed ( Figure 6C). During EMT, polarized epithelial cells rearrange cytoskeleton, dissolve the cell-cell junctions and convert into non-polarized mesenchymal cells [26][27][28]. Here we found that depletion of PNN changed the morphology from long, polygonal form to spindle appearances in PC-3 cells ( Figure 6D).…”

Section: Pnn Over-expression Induces Prostate Cancer Cell Emtmentioning

confidence: 56%

Pinin promotes tumor progression via PI3K/AKT/CREB signaling pathway in prostate cancer

Meng

Zhang²,

Ren

et al. 2020

Preprint

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Abstract Background Pinin (PNN), a desmosome associated protein, was demonstrated to be over-expressed and act as a tumor-promoting factor in ovarian cancer, hepatocellular carcinoma and colorectal cancer. However, the precise role of PNN in prostate cancer is still unknown. Methods The expression levels of PNN were assessed in prostate cancer by qRT-PCR, western blotting and immunohistochemical staining. The other proteins were quantified by western blotting. PNN-depleted cells were produced by infecting with lentivirus bearing short hairpin RNAs against PNN. PNN over-expression was performed by transfecting PNN expression vector. The proliferation of each cell line was assessed by MTS and colony formation assays. Tumors were induced on nude mice by injecting tumor cells subcutaneously. Apoptosis and cell cycle were evaluated by flow cytometry. Transwell and wound healing assay were performed to determined the ability of cell invasion and migration. The TCGA data were analyzed with GEPIA (Gene Expression Profiling Interactive Analysis) and GraphPad Prism. Results Here, we reported that PNN was upregulated in prostate cancer tissues and PNN expression was positively associated with Gleason score, tumor stage and tumor metastasis. PNN promoted cell growth and tumorigenicity in vitro and in vivo, and might modulate cell growth through driving G1/S transition via CDK6, CDK2, and Cyclin D1 in prostate cancer cells. Furthermore, PNN accelerated cell invasion, migration and EMT processes of prostate cancer cells accompanied with the up-regulation of MMP-2, MMP-9, N-cadherin, Vimentin and down-regulation of E-cadherin. Mechanism study demonstrated that the proliferation- and motility-promoting effects of PNN on prostate cancer cells dependent on the activation of PI3K/AKT/CREB signaling, which was reversed by AKT and CREB inhibitors. Conclusions Collectively, these findings indicated that PNN plays important roles in prostate cancer tumorigenesis and progression and it may be a potential therapeutic target for prostate cancer treatment.

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Section: Pnn Over-expression Induces Prostate Cancer Cell Emtmentioning

confidence: 56%

Pinin promotes tumor progression via PI3K/AKT/CREB signaling pathway in prostate cancer

Meng

Zhang²,

Ren

et al. 2020

Preprint

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“…Importantly, EMT is not a one‐way road but a highly dynamic and reversible process, providing cancer cells with the plasticity needed to cope with the different challenges on their way to distant metastasis formation (Chaffer et al , ). In addition to ZEB1, EMT can also be induced by other core EMT‐transcription factors (EMT‐TFs), namely ZEB2, TWIST1 and the two members of the Snail family, which most likely all have non‐redundant subfunctions (Stemmler et al , ; Yang et al , ). Notably, these core EMT‐TFs not only exert “classical” EMT properties, like loss of epithelial integrity and increased motility, but also confer other properties important for cancer progression, including stemness, survival and therapy resistance (Nieto et al , ).…”

Section: Introductionmentioning

confidence: 99%

Genome‐wide cooperation of EMT transcription factor ZEB 1 with YAP and AP ‐1 in breast cancer

et al. 2020

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Invasion, metastasis and therapy resistance are the major cause of cancer‐associated deaths, and the EMT‐inducing transcription factor ZEB1 is a crucial stimulator of these processes. While work on ZEB1 has mainly focused on its role as a transcriptional repressor, it can also act as a transcriptional activator. To further understand these two modes of action, we performed a genome‐wide ZEB1 binding study in triple‐negative breast cancer cells. We identified ZEB1 as a novel interactor of the AP‐1 factors FOSL1 and JUN and show that, together with the Hippo pathway effector YAP, they form a transactivation complex, predominantly activating tumour‐promoting genes, thereby synergising with its function as a repressor of epithelial genes. High expression of ZEB1, YAP, FOSL1 and JUN marks the aggressive claudin‐low subtype of breast cancer, indicating the translational relevance of our findings. Thus, our results link critical tumour‐promoting transcription factors: ZEB1, AP‐1 and Hippo pathway factors. Disturbing their molecular interaction may provide a promising treatment option for aggressive cancer types.

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“…The epithelial-mesenchymal transition (EMT) is an impactful cell behavior in normal and disease states in metazoans (Yang et al, 2020). Cell movements that are a product of EMT during embryonic development are essential to form numerous tissues and organs via mechanisms that are analogous to cell invasion during cancer metastasis Kerosuo and Bronner-Fraser, 2012;Theveneau and Mayor, 2012;Thiery et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

P-bodies are sites of rapid RNA decay during the neural crest epithelial—mesenchymal transition

Hutchins

Piacentino

Bronner

2020

Preprint

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The epithelial-mesenchymal transition (EMT) drives cellular movements during development to create specialized tissues and structures in metazoans, using mechanisms often coopted during metastasis. Neural crest cells are a multipotent stem cell population that undergo a developmentally regulated EMT and are prone to metastasis in the adult, providing an excellent model to study cell state changes and mechanisms underlying EMT. A hallmark of neural crest EMT during avian development is temporally restricted expression followed by rapid down-regulation of the Wnt antagonist Draxin. Using live RNA imaging, here we demonstrate that rapid clearance of Draxin transcripts is mediated post-transcriptionally via localization to processing bodies (P-bodies), small cytoplasmic granules which are established sites of RNA processing. Contrasting with recent work in immortalized cell lines suggesting that P-bodies are sites of storage rather than degradation, we show that targeted decay of Draxin occurs within P-bodies during neural crest migration. Furthermore, P-body disruption via DDX6 knockdown inhibits not only endogenous Draxin down-regulation but also neural crest EMT in vivo. Together, our data highlight a novel and important role for P-bodies in an intact organismal context−controlling a developmental EMT program via post-transcriptional target degradation.

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Guidelines and definitions for research on epithelial–mesenchymal transition

Cited by 1,257 publications

References 92 publications

Pinin promotes tumor progression via PI3K/AKT/CREB signaling pathway in prostate cancer

Pinin promotes tumor progression via PI3K/AKT/CREB signaling pathway in prostate cancer

Genome‐wide cooperation of EMT transcription factor ZEB 1 with YAP and AP ‐1 in breast cancer

P-bodies are sites of rapid RNA decay during the neural crest epithelial—mesenchymal transition

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