Vitamin D Deficiency has a Negative Impact on Cetuximab-Mediated Cellular Cytotoxicity against Human Colon Carcinoma Cells
Abstract
Background Hypovitaminosis D is associated with an adverse prognosis in colon cancer patients, possibly due to the effects of the vitamin on the immune system. Antibody-dependent cell-mediated cytotoxicity (ADCC) significantly contributes to the anti-tumor effects of monoclonal antibodies, including cetuximab, an epidermal growth factor receptor (EGFR)-targeted monoclonal antibody that is frequently added to chemotherapy in the treatment of colon cancer.Objective The present study evaluates the association between vitamin D serum levels and the ability of ex vivo NK cells to support cetuximab-mediated ADCC in colon cancer cell lines.Methods Blood samples were obtained from 124 healthy volunteers and serum vitamin D was determined by RIA. NK cells were isolated from each sample and added to human colorectal carcinoma cells with or without cetuximab, and ADCC was assessed using a colorimetric lactate dehydrogenase assay.Results Correlation analysis indicates a significant, gender- and age-independent association between vitamin D levels and cetuximab-induced ADCC on HT29 cells, where NK cells from samples with vitamin D < 20 ng/mL are significantly less efficient in inducing ADCC. A confirmatory study on two additional colon cancer cell lines yielded similar results.Conclusions These data suggest that vitamin D supplementation in vitamin-deficient/insufficient colorectal cancer patients could improve cetuximab-induced ADCC.
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Supplementation with vitamin D in vitamin-deficient/insufficient CRC cells has been suggested to improve cetuximab-induced ADCC in CRC cell lines.
“Supplementation with vitamin D in vitamin-deficient/insufficient CRC cells has been suggested to improve cetuximab-induced ADCC in CRC cell lines [136].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [136]
Vitamin D deficiency has a negative impact on cetuximab-induced ADCC.
“In addition, vitamin D deficiency has a negative impact on cetuximab-induced ADCC.”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [136]
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Self-citation
- Authors
- Mortara, L., Gariboldi, M. B., Bosi, A., Bregni, M., Pinotti, G., Guasti, L., Squizzato, A., Noonan, D. M., Monti, E., & Campiotti, L.
- Affiliations
- University of Insubria (IT)
- Azienda Socio Sanitaria Territoriale della Valle Olona (IT)
- Aziende Socio Sanitarie Territoriale dei Sette Laghi (IT)
- Corresponding author
- Monti, Elena
- ORCID
- Venue
- Targeted Oncology
- Published
- 2018-08-09
- Volume
- 13
- Issue
- 5
- Pages
- 657-665
- ISSN
- 1776-2596 (ISSN-L)
- 1776-260X
- OpenAlex
- W2885688630
- Cited by
- 18
- References
- 50
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 1 · 2019: 3
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Targeted Oncology (publishedVersion)
- PubMed (publishedVersion)
- IrInSubria (University of Insubria) (submittedVersion)
- Funders
- AIRC - Associazione Italiana per la Ricerca contro il CANCRO (AIRC- IG15895)
- Università dell'Insubria - Fondo di Ateneo per la Ricerca (FAR2014, FAR 2015)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- vitamin D deficiency, cetuximab, antibody-dependent cellular cytotoxicity, natural killer cells, colon cancer, colorectal cancer, epidermal growth factor receptor, serum vitamin D levels, vitamin D supplementation, HT-29 cells, lactate dehydrogenase assay
- MeSH terms
- Cetuximab, Colonic Neoplasms, Female, Humans, Male, Middle Aged, Vitamin D Deficiency, Cell Line, Tumor
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