Expression of hypoxia inducible factor 1α and 2α and its association with vitamin C level in thyroid lesions
Open accessAbstract
BACKGROUND: Cells adapt to hypoxia by transcriptional induction of genes that participate in regulation of angiogenesis, glucose metabolism and cell proliferation. The primary factors mediating cell response to low oxygen tension are hypoxia inducible factors (HIFs), oxygen-dependent transcription activators. The stability and activity of the α subunits of HIFs are controlled by hydroxylation reactions that require ascorbate as a cofactor. Therefore, deficiency of intracellular vitamin C could contribute to HIFs overactivation. In this study, we investigated whether vitamin C content of human thyroid lesions is associated with HIF-1α and HIF-2α protein levels. METHODS: Expression of HIF-1α and HIF-2α as well as vitamin C content was analyzed in thyroid lesions and cultured thyroid carcinoma cell lines (FTC-133 and 8305c) treated with hypoxia-mimetic agent (cobalt chloride) and ascorbic acid. The expression of HIFs and hypoxia-induced glucose transporters were determined by Western blots while quantitative real-time PCR (qRT-PCR) was performed to detect HIFs mRNA levels. Ascorbate and dehydroascorbate levels were measured by HPLC method. RESULTS: We found an inverse correlation between vitamin C level and HIF-1α but not HIF-2α expression in thyroid lesions. These results agree with our in vitro study showing that vitamin C induced a dose - dependent decrease of HIF-1α but not HIF-2α protein level in thyroid cancer cells FTC-133 and 8305C. The decreased HIF-1α expression was correlated with reduced expression of hypoxia-related glucose transporter 1 (GLUT1) in thyroid cancer cells. CONCLUSION: The results demonstrate that HIF-1α activation is associated with vitamin C content in thyroid lesions. Our study suggests that high tumor tissue ascorbate level could limit the expression of HIF-1α and its targets in thyroid lesions.
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Low concentrations of ascorbic acid (25 mM) suppress HIF-1α expression in hypoxic conditions, subsequently impeding tumor growth.
“Similarly, low concentrations of ascorbic acid (25 mM) have been shown to suppress HIF-1α expression in hypoxic conditions, subsequently impeding tumor growth.301”
From Drug repurposing for cancer therapy (2024) · cites this paper as [301]
The Results section (page unavailable) reports that ascorbic acid reduced HIF-1α protein levels in thyroid cancer cells under cobalt-chloride-induced, hypoxia-mimicking conditions. But the tested concentrations were 0.1–1 mM, not 25 mM, and the study did not show that this HIF-1α reduction subsequently impeded tumor growth. The Background mentions reduced tumor growth in mice as a finding from another study, without establishing the claimed causal sequence. (LLM, conf=0.91)
Experimental — accuracy not yet measuredAscorbic acid induces a dose-dependent decrease in expression of HIF-1α and GLUT1 in thyroid cancer cells in vitro.
“Furthermore, ascorbic acid has been shown to induce a dose-dependent decrease in the expression of HIF-1α and GLUT1, both identified as downstream targets of HIF-1, in thyroid cancer cells in vitro.”
From Drug repurposing for cancer therapy (2024) · cites this paper as [301]
In thyroid lesions, ascorbate levels were inversely related to HIF1α expression, and ascorbate lowered HIF1α and GLUT1 in thyroid cancer cells in a dose-dependent way.
“Ascorbate level was inversely correlated with HIF1α expression in thyroid lesions80, and in vitro study showed that ascorbate treatment induced a dose-dependent decrease in expression of HIF1α and GLUT1 (a downstream target of HIF 1) in thyroid cancer cells80.”
From Targeting cancer vulnerabilities with high-dose vitamin C (2019) · cites this paper as [80]
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- Authors
- Jóźwiak, P., Ciesielski, P., Zaczek, A., Lipińska, A., Pomorski, L., Wieczorek, M., Bryś, M., Forma, E., & Krześlak, A.
- Affiliations
- University of Łódź (PL)
- Medical University of Lodz (PL)
- Corresponding author
- Krześlak, Anna
- ORCID
- Venue
- Journal of Biomedical Science
- Published
- 2017-10-30
- Volume
- 24
- Issue
- 1
- Pages
- 83-83
- ISSN
- 1021-7770 (ISSN-L)
- 1423-0127
- PMC
- PMC5663109
- OpenAlex
- W2766096623
- Cited by
- 31
- References
- 44
- Citations by year
- 2025: 4 · 2024: 4 · 2023: 3 · 2022: 6 · 2021: 7 · 2020: 2 · 2019: 2 · 2018: 3
- FWCI
- 0.64
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Journal of Biomedical Science (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- statutory funds of University of Lodz
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Nursing › Nutrition and Dietetics › Vitamin C and Antioxidants Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Keywords
- hypoxia-inducible factor-1α, HIF-2α, vitamin C, thyroid lesions, thyroid cancer, hypoxia, cobalt chloride, glucose transporter 1, ascorbate deficiency, tumor hypoxia
- MeSH terms
- Endothelial PAS Domain-Containing Protein 1, Adult, Aged, Ascorbic Acid Deficiency, Dehydroascorbic Acid, Female, Humans, Male, Middle Aged, Poland, Thyroid Gland, Thyroid Neoplasms, Vitamins, Cell Line, Tumor, Basic Helix-Loop-Helix Proteins, Basic Helix-Loop-Helix Transcription Factors, Hypoxia-Inducible Factor 1, alpha Subunit
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