Direct regulation of TWIST by HIF-1α promotes metastasis

By Muh-Hwa Yang, Min-Zu Wu, S. Chiou, Po-min Chen, Shyue-Yih Chang, Chung-Ji Liu, S. Teng, Kou-Juey Wu. Nature Cell Biology, 2008

969 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/c2cc09d847d153b6fe606770df6c2afa9d3196ea

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Citations in the corpus

Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition (2010, background): “Co-overexpression of HIF-1α, Twist1 and Snail in HNSCC correlates with the worst prognosi”
PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation to promote metastasis (2014, background): “Focal hypoxia may induce an EMT program(16, 26), and our results indicate that while cancer cells acquire a mesenchymal phenotype (EMT) independently of PGC-1α-induced pathways, both pathways coexist and are associated with cancer cell migration, invasion and metastasis(27).”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “Interestingly, in addition to inducing TGF-b1, HIF-1a can also directly activate the expression of EMT inducers Snail, Twist and the members of the Zeb family (Evans et al, 2007; Krishnamachary et al, 2006; Sun et al, 2009; Yang et al, 2008) (Fig 3).”
Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “Hypoxic responses mediated by HIF-1 were also shown to induce the expression of Twist1 and Snail1 to promote EMT (Yang et al. 2008; Mak et al. 2010).”
The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, methodology): “Furthermore, Gata3 promotes the EMT in lung carcinomas (Yang et al. 2011), whereas it is downregulated in renal carcinomas with EMT signatures and inhibits breast cancer metastasis through the induction of the MET (Tun et al. 2010, Yan et al. 2010).”
Transcriptional Regulation by Hypoxia Inducible Factors (2013, background): “…(POU5F1), as well as many genes that are involved in epithelial to mesenchymal transition (EMT) during development and utilized by cancer cells in metastasis and invasion such as LOX, MMP1 and TWIST (Covello et al., 2006; Erler et al., 2006; Petrella et al., 2005; Semenza, 2012; Yang et al., 2008).”
Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “Activated HIF 1 a or HIF 2 a directly or indirectly regulate SNAI 1 , TWIST 1 and ZEB 1 expression which fosters stemness and metastasis formation in bladder, ovarian, gastric and breast cancer (Yang et al , 2008 ; Cooke et al , 2012 ; Liu et al , 2017 ; Hapke & Haake, 2020 ; Zhang et al , 2020 ).”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “HIF-1α is capable of binding directly to the hypoxiα-responsive element of the TWIST1 promoter (238).”
The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “towards EMT and the tumor cell invasion (Yang et al., 2008).”
Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “Twist expression can be activated by hypoxia-inducible factor 1α (HIF1α) transcription factor under hypoxic conditions to promote EMT and metastasis (Yang et al., 2008).”
Tumor cell metabolism: cancer's Achilles' heel. (2008, background): “HIF-1a activation also causes the expression of the met proto-oncogene and of TWIST, both of which favor EMT (Pennacchietti et al., 2003; Yang et al., 2008), and induces two proteins that play a cardinal role in metastasis, the chemokine receptor CXCR4 (Igney and Krammer, 2002) and lysyl oxidase…”