Hypoxia-inducible factor 1a (HIF-1a), a key regulator of cancer metabolism, migration and angiogenesis that is stably expressed in RCCs by virtue of a genetic mutation in the von Hippel-Lindau (VHL) tumor-suppressor protein, was impeded by auraptene, which blocked HIF-1a translation initiation without causing cytotoxicity.
Thus, our results indicate that testis-specific form of PFKFB or PFK-2/FBPase-2 is also expressed in several cancer cell lines and that hypoxia induces transcription of PFKFB4 gene in these cell lines by HIF-1alpha dependent mechanism.
Male, but not female, SART1(+/-) mice showed significant up-regulation of HIF-1α in circulating and liver-infiltrating immune cells, but not in hepatocytes, before development of malignancy.
No mutations seem to occur in the ODD of hif-1alpha in HIF-1alpha overexpressing invasive breast cancer, which rules ODD mutations out as a possible explanation for the diffuse HIF-1alpha expression pattern often seen in this cancer.
The results from the published studies on the association between hypoxia-inducible factor-1(Hif-1/HIF-1) polymorphisms and cancer risk are conflicting.
After an appropriate number of cancer tissues were taken, the experimental group was treated with oral administration of 500 mg vitamin B3 every day, while the placebo group was treated with oral administration of the same amount of placebo; after 1 week, the skin cancer tissues in the same part were taken, and the skin tissues of healthy people were taken as the control group; the mRNA and protein expression levels of HIF-1α and p53 in tissues were detected.
HIF-1α regulates the expression of a series of genes, which are involved in cell proliferation, differentiation, apoptosis, angiogenesis, migration and invasion and represents a potential therapeutic target for the treatment of human cancer.
Over-expression of HIF1α caused by intratumoral hypoxia and its genetic alterations are associated with increased mortality in several cancer types including non-small-cell lung cancer (NSCLC).
The seven in absentia homolog 2 (SIAH2) protein plays a significant role in human cancer by regulating hypoxia-inducible factor-a (HIF-1α); however, its role in T-cell acute lymphoblastic leukemia (T-ALL) is less clear.
These findings reveal an ERK-controlled, unconventional and anti-apoptotic function of HIF-1α that might serve as an early protective mechanism upon oxygen limitation and promote cancer cell resistance to chemotherapy.
Does endogenous fatty acid metabolism allow cancer cells to sense hypoxia and mediate hypoxic vasodilatation? Characterization of a novel molecular connection between fatty acid synthase (FAS) and hypoxia-inducible factor-1alpha (HIF-1alpha)-related expression of vascular endothelial growth factor (VEGF) in cancer cells overexpressing her-2/neu oncogene.
This review summarises the experimental evidence of the crosstalk between HIF-1 and specific calcium channels, pumps and regulators in the context of cancer.
Identifying the role of STAT3 in the hypoxia response provides further data supporting the effectiveness of STAT3 inhibitors in solid tumor treatment owing to their usefulness in inhibiting both the STAT3 and HIF1 pro-tumorigenic signaling pathways in some cancer types.
In this review, we summarize the recent information on HIF-1α in gastric cancer with special focus on the mechanism underlying HIF-1α signaling effects on proliferation, apoptosis, angiogenesis, EMT and drug-resistance of cancer cells, thereby predicting new therapeutic agents for better management of this malignancy.
Hypoxic conditions in the pancreatic tumor microenvironment lead to the stabilization of hypoxia-inducible factor-1 alpha (HIF-1α), which acts as the master regulator of cancer cell metabolism.