About this Research Topic
Hypoxia is a pathological hallmark of many human diseases, including cancer. For decades, tumor hypoxia has been considered a major culprit in disease progression and treatment resistance. This is because hypoxia or oncogenic mutations activate hypoxia-inducible factors, including HIF1 and HIF2, which in turn serve as master transcriptional factors for the upregulation of diverse groups of genes and pathways. Many of the hypoxia response genes support cellular stress adaptation and survival, and this feature is “hijacked” by cancer cells. Thus, hypoxic cancer cells are more likely to survive and grow compared to their normoxic counterparts. However, there are still significant gaps in our molecular and pathological knowledge in how hypoxia promotes cancer progression and treatment resistance. Currently, there is no clinically approved approach to specifically target tumor hypoxia.
Cancer development is driven by multiple genetic and epigenetic alterations. However, the functional roles of hypoxia in promoting tumor growth and therapy resistance within the context of these alterations are not entirely clear. The goal of this Research Topic is to showcase our recent understanding in how the hypoxia response pathway interacts with these alterations (e.g. Myc, RAS, and androgen receptor), the functional consequences of these interactions to tumor cell activities (e.g. metabolism, invasion, and immunity), and the clinical significance to disease outcome (e.g. disease progression, and treatment sensitivity and resistance).
In particular, we welcome articles falling under the following points:
• HIF post-translational modification and protein-protein interaction
• Genes that are co-regulated by hypoxia and other oncogenic pathways (e.g. PI3K, RAS or Myc)
• System and computational biology to dissect the crosstalk of HIF and other oncogenic pathways
• Determination and quantification the hypoxic effect in a heterogeneous tumor
Keywords: Hypoxia, HIF, Oncogenic Signaling, Crosstalk, Treatment Resistance
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