The EMT-activator Zeb1 is a key factor for cell plasticity and promotes metastasis in pancreatic cancer

By A. Krebs, J. Mitschke, María Lasierra Losada, O. Schmalhofer, Melanie Boerries, H. Busch, M. Boettcher, Dimitrios Mougiakakos, W. Reichardt, P. Bronsert and 6 more. Nature Cell Biology, 2017

877 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/68da0d50e5a2441d2876495f2a18e6d240f147a1

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In Molecular Biology

1. Wei Dang Lu
2. Yibin Kang
3. M. Bahar
4. D. Kim
5. Hyun Joon Kim
6. Yuhe Huang
7. Raghu Kalluri
8. Yongsheng Li

In Oncology

1. Wei Dang Lu
2. Yibin Kang
3. Yuhe Huang
4. A. Rustgi
5. Raghu Kalluri
6. Yongsheng Li
7. Dingshan Li
8. Xiawei Wei

Citations in the corpus

• Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “278 Based on previous studies, MAPK signaling, autophagy, and EMT are physically and functionally interconnected during cancer metastasis (Fig.”
• The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “In addition, the EMT-TFs have the ability to modulate each other in a complex, dynamic and interdependent manner.”
• EMT, MET, plasticity and tumor metastasis (2020, background): “While Snail or Twist is dispensable individually, Zeb1 knockout in the same genetic background impairs multiple stages of tumorigenesis, ranging from premalignant lesions to metastatic tumors [27].”
• The interaction between ferroptosis and lipid metabolism in cancer (2020, background): “In addition, a systematic study of cellular responses to ferroptosis inducer revealed that high mesenchymal state is associated with zinc-finger E-box binding homeobox 1 (ZEB1), a transcription factor reported to be a central regulator of lipid metabolism and adipogenic fate and can enhance stemness”
• Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “In contrast, ZEB1 is a strong promoter of metastasis in the same pancreatic cancer model (Krebs et al., 2017) (Figure 3A).”
• Dynamic EMT: a multi‐tool for tumor progression (2021, neutral): “ZEB1 deficient pancreatic cancer cell lines are incapable of compensatory increasing glycolysis when oxidative phosphorylation is blocked, highlighting poor glycolytic reserve (Krebs et al , 2017).”
• Systems Biology of Cancer Metastasis (2019, result): “In contrast, recent reports indicate that the EMT transcription factor, Zeb1 is required for pancreatic tumor metastasis(Krebs et al., 2017), and that post-EMT mesenchymal-like cells cooperate with epithelial cells to eventually become metastatic by paracrine signaling(Neelakantan et al., 2017).”