Here, the interplay between MYC and HIF will be reviewed in the context of the normal cellular homeostatic response versus the collaboration of HIF and oncogenic MYC in cancer.

In this review, we summarize the effects of c-Myc and HIFs on carbon metabolism, protein synthesis, and proliferation, highlighting their antagonist effects on carbon utilization and translation initiation. We will also describe direct effects of HIFs on c-Myc transcriptional activity.

The ability of cells to grow during hypoxia results in part from crosstalk between hypoxia-inducible factors (HIFs) and the proto-oncogene c-Myc. Acting alone, HIF and c-Myc partially regulate complex adaptations undertaken by tumor cells growing in low O(2).

Specifically, under hypoxic conditions HIF-1-mediated regulation of oncogenic c-Myc plays a pivotal role in conferring metabolic advantages to tumor cells as well as adaptation to the tumorigenic micromilieu.

Nov 5, 2020 · Earlier studies focused on the inhibition of MYC by HIF during hypoxia, when MYC is expressed at physiological level, to help cells survive under low oxygen conditions. Emerging evidence suggests that MYC and HIF also cooperate to …

Jan 11, 2008 · HIF-1 α regulates hypoxia-responsive gene expression through c-Myc displacement. (a) c-Myc acts as a repressor by binding to Miz1 at the initiator element (INR) of the CDKN1A gene in...

When MYC-dependent tumors grow, the hypoxic tumor microenvironment elevates the levels of HIF, such that oncogenic MYC and HIF collaborate to enhance the cancer cell's metabolic needs through increased uptake of glucose and its conversion to lactate.

As hypoxia signals a cellular deprivation state, HIF-1 has also been reported to counter the activity of MYC, which encodes a transcription factor that drives cell growth and proliferation.

The interaction of MYC and hypoxia inducible factors (HIFs) under physiological, non-tumorigenic conditions provides insights into normal homeostatic cellular responses to low oxygen levels (hypoxia).

Aug 8, 2019 · MYC through HIF-2α maintains self-renewal in human lymphoma. To confirm our findings from transgenic mouse model system in a human equivalent tumor, we first identified the equivalent ABCG2+/HIF-2α CSC subpopulation in relapsed cases of human adult Acute Lymphoblastic Lymphoma (T-LBL).