L-Ascorbic acid can abrogate SVCT-2-dependent cetuximab resistance mediated by mutant KRAS in human colon cancer cells
Abstract
Colon cancer patients with mutant KRAS are resistant to cetuximab, an antibody directed against the epidermal growth factor receptor, which is an effective clinical therapy for patients with wild-type KRAS. Numerous combinatorial therapies have been tested to overcome the resistance to cetuximab. However, no combinations have been found that can be used as effective therapeutic strategies. In this study, we demonstrate that L-ascorbic acid partners with cetuximab to induce killing effects, which are influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human colon cancer cells with a mutant KRAS. L-Ascorbic acid treatment of human colon cancer cells that express a mutant KRAS differentially and synergistically induced cell death with cetuximab in a SVCT-2-dependent manner. The ectopic expression of SVCT-2 induced sensitivity to L-ascorbic acid treatment in human colon cancer cells that do not express SVCT-2, whereas the knockdown of endogenous SVCT-2 induced resistance to L-ascorbic acid treatment in SVCT-2-positive cells. Moreover, tumor regression via the administration of L-ascorbic acid and cetuximab in mice bearing tumor cell xenografts corresponded to SVCT-2 protein levels. Interestingly, cell death induced by the combination of L-ascorbic acid and cetuximab resulted in both apoptotic and necrotic cell death. These cell death mechanisms were related to a disruption of the ERK pathway and were represented by the impaired activation of RAFs and the activation of the ASK-1-p38 pathway. Taken together, these results suggest that resistance to cetuximab in human colon cancer patients with a mutant KRAS can be bypassed by L-ascorbic acid in an SVCT-2-dependent manner. Furthermore, SVCT-2 in mutant KRAS colon cancer may act as a potent marker for potentiating L-ascorbic acid co-treatment with cetuximab.
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Resistance to cetuximab in colorectal cancer cells with KRAS mutations can be bypassed by L-ascorbic acid relying on a sodium-dependent vitamin C transporter 2.
“Jung revealed that resistance to cetuximab in CRC cells with KRAS mutations can be bypassed by L-ascorbic acid relying on a sodium-dependent vitamin C transporter 2 [51].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [51]
Resistance to cetuximab in mutant KRAS CRC patients can be reversed by L-ascorbic acid by reducing RAF/ERK activity in an SVCT-2-dependent manner.
“Resistance to cetuximab in mutant KRAS CRC patients can be reversed by L-ascorbic acid by reducing RAF/ERK activity in an SVCT-2-dependent manner [51].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [51]
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- Authors
- Jung, S.-A., Lee, D.-H., Moon, J.-H., Hong, S.-W., Shin, J.-S., Hwang, I. Y., Shin, Y. J., Kim, J. H., Gong, E.-Y., Kim, S.-M., Lee, E. Y., Lee, S., Kim, J. E., Kim, K.-P., Hong, Y. S., Lee, J. S., Jin, D.-H., Kim, T., & Lee, W. J.
- Affiliations
- Asan Medical Center (KR)
- Seoul National University (KR)
- Corresponding author
- Jin, Dong-Hoon
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 95
- Pages
- 200-208
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2307614550
- Cited by
- 47
- References
- 25
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 7 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 7 · 2017: 3 · 2016: 2
- FWCI
- 2.87
- Type
- journal article
- Language
- en
- Update notices
- erratum (2016-08-01)
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Health and Welfare (HI06C0868, 1420030)
- National Research Foundation of Korea
- Ministry of Education, Science and Technology (2013R1A2A2A01067394)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Nursing › Nutrition and Dietetics › Vitamin C and Antioxidants Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- vitamin C, cetuximab resistance, mutant KRAS, colon cancer, SVCT2, anti-EGFR therapy, combination therapy, apoptosis, necrosis, ERK signaling, Raf, ASK1, p38 MAPK, tumor xenografts, biomarkers
- MeSH terms
- Cetuximab, Animals, Ascorbic Acid, Colonic Neoplasms, Drug Synergism, Humans, Proto-Oncogene Proteins p21(ras), Drug Resistance, Neoplasm, MAP Kinase Signaling System, Xenograft Model Antitumor Assays, Cell Line, Tumor, Cell Proliferation, Mice, Sodium-Coupled Vitamin C Transporters, ErbB Receptors
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