ReviewAdvances in experimental medicine and biology2021
HIF-1α Metabolic Pathways in Human Cancer.
Review in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- MicroRNA-486: a dual-function biomarker for diagnosis and tumor immune microenvironment characterization in non-small cell lung cancer.BMC medical genomics · 2025Pooled it
- Metabolic Modulation in Cancer Care: The Potential Role of Glucagon-Like Peptide-1 Receptor Agonists.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026Review
- The Many Faces of SetDB1.Epigenomes · 2026Review
- UHRF1 silencing restrained the malignant phenotype of melanoma cells by inhibiting the HOXA9/HIF-1α axis-mediated glycolysis.European journal of medical research · 2025Article
- Curcumol Targets the VHL/HIF-1α Axis to Suppress Glycolysis-Driven Progression in Colorectal Cancer.Cancers · 2025Article
- HIF-1α Promotes the Confined Migration of Gastric Cancer Cells by Modulating Phosphatidylcholine Metabolism.Journal of cellular and molecular medicine · 2025Article
- Mitochondrial ROS and HIF-1α signaling mediate synaptic plasticity in the critical period.PLoS biology · 2025Article
- Association of Lutein with Cancer: A Systematic Review of the Lutein Effects on Cellular Processes Involved in Cancer Progression.Preventive nutrition and food science · 2025Article
- Targeting hypoxia-induced HIF-1α/JMJD3/Notch axis in gastric cancer therapy.Journal of bioenergetics and biomembranes · 2025Article
- Small-molecule RNA therapeutics to target prostate cancer.Cancer cell · 2025Article
- Impact of glycolysis enzymes and metabolites in regulating DNA damage repair in tumorigenesis and therapy.Cell communication and signaling : CCS · 2025Review
- FOSL1 transcriptionally dictates the Warburg effect and enhances chemoresistance in triple-negative breast cancer.Journal of translational medicine · 2025Article
- Effects of serum HIF-1α, VEGF, and uPA levels on clinicopathologic findings and prognosis in oral squamous cell carcinoma.International journal of clinical and experimental pathology · 2025Article
- Hypoxia-induced BNIP3 facilitates the progression and metastasis of uveal melanoma by driving metabolic reprogramming.Autophagy · 2025Article
- SELENBP1 Inhibits the Warburg Effect and Tumor Growth by Reducing the HIF1α Expression in Colorectal Cancer.Current cancer drug targets · 2025Article
- Emerging Therapeutic Targets in Rheumatoid Arthritis: Focusing on HIF-1α, Nrf2, STATs, and RORγt.Current drug targets · 2025Review
- Article
- Genistein inhibits HIF-1α and attenuates high glucose-induced peritoneal mesothelial-mesenchymal transition and fibrosis via the mTOR/OGT pathway.Scientific reports · 2024Article
- Prognostic value of combining clinical factors,Annals of nuclear medicine · 2024Article
- Adjuvant Properties of Caffeic Acid in Cancer Treatment.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxygen is directly involved in many key pathophysiological processes. Oxygen deficiency, also known as hypoxia, could have adverse effects on mammalian cells, with ischemia in vital tissues being the most significant (Michiels C. Physiological and pathological responses to hypoxia. Am J Pathol 164(6): 1875-1882, 2004); therefore, timely adaptive responses to variations in oxygen availability are essential for cellular homeostasis and survival. The most critical molecular event in hypoxic response is the activation and stabilization of a transcriptional factor termed hypoxia-induced factor-1 (HIF-1) that is responsible for the upregulation of many downstream effector genes, collectively known as hypoxia-responsive genes. Multiple key biological pathways such as proliferation, energy metabolism, invasion, and metastasis are governed by these genes; thus, HIF-1-mediated pathways are equally pivotal in both physiology and pathology.As we gain knowledge on the molecular mechanisms underlying the regulation of HIF-1, a great focus has been placed on elucidating the cellular function of HIF-1, particularly the role of HIF-1 in cancer pathogenesis pathways such as proliferation, invasion, angiogenesis, and metastasis. In cancer, HIF-1 is directly involved in the shift of cancer tissues from oxidative phosphorylation to aerobic glycolysis, a phenomenon known as the Warburg effect. Although targeting HIF-1 as a cancer therapy seems like an extremely rational approach, owing to the complex network of its downstream effector genes, the development of specific HIF-1 inhibitors with fewer side effects and more specificity has not been achieved. Therefore, in this review, we provide a brief background about the function of HIF proteins in hypoxia response with a special emphasis on the unique role played by HIF-1α in cancer growth and invasiveness, in the hypoxia response context.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.