Notch signaling mediates hypoxia-induced tumor cell migration and invasion

By C. Sahlgren, M. Gustafsson, Shaobo Jin, L. Poellinger, U. Lendahl. Proceedings of the National Academy of Sciences of the United States of America, 2008

852 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3e041baa8070aa0764f21155e7d4b6eac15c874e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. M. Nieto
2. R. Weinberg
3. J. P. Thiery
4. R. Huang
5. J. López-Novoa
6. K. Polyak
7. J. Espinosa
8. Yibin Kang

In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. J. P. Thiery
4. D. Medici
5. David M. Gonzalez
6. Yibin Kang
7. R. Huang
8. A. Capobianco

Citations in the corpus

• Angiogenic signaling pathways and anti-angiogenic therapy for cancer (2023, background): “In tumor models, EMT and invasion induced by hypoxia could be offset after suppressing the Notch signaling pathway.(295) Notch-Dll/Jag is an indispensable pathway in the initial stage of physiological and pathological angiogenesis with visible advantages in anti-tumor therapy, but its complex mechan”
• Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “Indeed, several signaling pathways including Wnt, Notch and nuclear factor-κB (NF-κB) signaling increase SNAI1 activity and induce EMT by inactivating GSK3β-mediated phosphorylation (Sahlgren et al., 2008; Wu et al., 2009; Yook et al., 2006).”
• Notch signalling in solid tumours: a little bit of everything but not all the time (2011, background): “Blocking either HIF or the Notch co-activator MAML1 in breast, colon or cervical cancer cells reduced the invasion and metastatic ability of these cell”
• Hypoxia-inducible factors in stem cells and cancer (2009, neutral): “4324 HIF-1 mediated hypoxic epithelial–mesenchymal transition of tumour cells [82], and development of thymic lymphomas [83].”
• The Role of Snail in EMT and Tumorigenesis (2013, background): “Notch increases LOX expression by recruiting hypoxia-inducible factor 1α (HIF-1α) to LOX promoter, which stabilizes Snail protein and results in up-regulation of EMT and the migration and invasion of cancer cells [39,40].”
• Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Additionally, binding of MMP3 induces the expression of RAC1 and increases the production of ROS and Snail1 (258, 259), which activate EMTand lead to production of other MMPs, such as MMP-2 and MMP-9.”
• Targeting cancer stem cell pathways for cancer therapy (2020, background): “206 Hypoxia-induced Jagged 2 activation enhances cell invasion of breast CSCs 207 and lung CSCs.”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “Interestingly, Notch directly promotes Snail1 activation during hypoxia through the binding of its processed intracellular form to the Snail promoter and the activation of Lox2 expression by the hypoxia factor 1 (HIF-1), thereby stabilizing the Snail1 protein (Sahlgren et al., 2008).”
• Oxygen in stem cell biology: a critical component of the stem cell niche. (2010, background): “When Notch signaling was shown to be required for hypoxia to maintain an undifferentiated state (Gustafsson et al., 2005), several groups began to question whether Notch signaling mediated hypoxia-induced EMT (Sahlgren et al., 2008).”
• Acquisition of Epithelial-Mesenchymal Transition phenotype of gemcitabine-resistant pancreatic cancer cells is linked with activation of Notch signaling pathway (2009, background): “Moreover, Notch potentiates hypoxia-inducible factor-1a recruitment to the lysyl oxidase promoter and elevates the hypoxia-induced up-regulation of lysyl oxidase, which stabilizes the Snail protein (28).”
• Notch signaling: simplicity in design, versatility in function (2011, background): “The binding of Notch ICD to HIF1 leads to the recruitment of HIF1 to Notch-responsive genes (Gustafsson et al., 2005; Sahlgren et al., 2008).”
• Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “A tantalizing possibility nevertheless, it remains to be tested both experimentally and via a theoretical model of the coupled core EMT circuit and Notch-Delta-Jagged signaling via interactions such as miR-200 inhibits Jagged (183), miR-34 inhibits Delta and Notch (184,185), and NICD activates SNAIL”
• Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits (2009, background): “In another study, the activation of Notch signalling was required for hypoxia-induced EM”