Related Experiment Video
Updated: Apr 28, 2026

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis
Published on: December 9, 2016
Hypoxia signaling and the metastatic phenotype
H Mujcic, R P Hill, M Koritzinsky
1Princess Margaret Cancer Centre and Campbell Family Institute for Cancer Research, University Health Network, 610 University Ave, Toronto, ON M5G 2M9, Canada. bwouters@uhnresearch.ca.
Poor oxygen (hypoxia) in tumors drives cancer spread. While hypoxia-inducible factors (HIFs) were studied, new research shows the unfolded protein response (UPR) also significantly promotes tumor metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Hypoxia is common in solid tumors, linked to poor prognosis and treatment resistance.
- Hypoxia triggers signaling pathways like HIF1/2 and UPR, promoting cancer cell adaptation and survival.
- These pathways can alter gene expression, influencing cancer cell metastasis.
Purpose of the Study:
- To investigate hypoxia-induced signaling pathways that promote tumor metastasis.
- To explore the role of the unfolded protein response (UPR) in hypoxia-mediated metastasis, beyond the established HIF pathway.
Main Methods:
- Analysis of signaling pathways activated by tumor hypoxia.
- Investigation of gene expression and cellular phenotype changes under hypoxic conditions.
- Focus on the contribution of UPR activation to cancer cell metastasis.
Main Results:
- Hypoxia activates HIF1/2 and UPR signaling pathways in tumor cells.
- These pathways induce changes promoting cancer cell adaptation and survival.
- Recent evidence highlights UPR activation as a key mediator of hypoxia-driven metastasis.
Conclusions:
- Hypoxia significantly impacts tumor malignancy and metastasis.
- Both HIF and UPR pathways are critical in mediating hypoxia-induced metastasis.
- Understanding UPR's role offers new therapeutic targets for preventing cancer spread.
Related Concept Videos
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Regulation of Angiogenesis and Blood Supply
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
The Tumor Microenvironment
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

