ArticleBritish journal of cancer2016
FOXO3a and the MAPK p38 are activated by cetuximab to induce cell death and inhibit cell proliferation and their expression predicts cetuximab efficacy in colorectal cancer.
Article in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Shared genetic architecture between the topology of brain white matter structural connectome and fluid intelligence.Communications biology · 2026Article
- Circulating Butyrate Attenuates Cetuximab Efficacy in Colorectal Cancer Through EGFR and AMPK-Wip1 Signaling.Drug design, development and therapy · 2026Article
- p38 Regulates FoxO3a-Mediated SOD2 Expression to Prevent Cd-Induced Oxidative Stress in Neuronal Cells.International journal of molecular sciences · 2025Article
- Engineered multifunctional transforming growth factor-β type II receptor ectodomain fusions for oncology applications.Frontiers in oncology · 2025Article
- Cynaropicrin induces the apoptosis of colorectal cancer cells by elevating reactive oxygen species and activating the JNK/p38 MAPK.American journal of cancer research · 2025Article
- Article
- Activation of p38 and JNK by ROS Contributes to Deoxybouvardin-Mediated Intrinsic Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Fangji Fuling Decoction Alleviates Sepsis by Blocking MAPK14/FOXO3A Signaling Pathway.Chinese journal of integrative medicine · 2024Article
- FOXO3a-interacting proteins' involvement in cancer: a review.Molecular biology reports · 2024Review
- Title Expression of FOXO3 and MAPK1 Genes in Patients with Benign Salivary Gland Tumors.Journal of clinical medicine · 2023Article
- P2YCancers · 2022Article
- Ag120-Mediated Inhibition of ASCT2-Dependent Glutamine Transport has an Anti-Tumor Effect on Colorectal Cancer Cells.Frontiers in pharmacology · 2022Article
- Inhibition of Prostaglandin E2 Receptor EP3 Attenuates Oxidative Stress and Neuronal Apoptosis Partially by Modulating p38MAPK/FOXO3/Mul1/Mfn2 Pathway after Subarachnoid Hemorrhage in Rats.Oxidative medicine and cellular longevity · 2022Article
- Cetuximab promotes RSL3-induced ferroptosis by suppressing the Nrf2/HO-1 signalling pathway in KRAS mutant colorectal cancer.Cell death & disease · 2021Article
- Activation of matrix metalloproteinases and FoxO3a in HaCaT keratinocytes by radiofrequency electromagnetic field exposure.Scientific reports · 2021Article
- MAGI1 inhibits the AMOTL2/p38 stress pathway and prevents luminal breast tumorigenesis.Scientific reports · 2021Article
- Transcription factors in colorectal cancer: molecular mechanism and therapeutic implications.Oncogene · 2021Review
- MAP17 contributes to non-small cell lung cancer progression via suppressing miR-27a-3p expression and p38 signaling pathway.Cancer biology & therapy · 2021Article
- Restricting Glutamine Uptake Enhances NSCLC Sensitivity to Third-Generation EGFR-TKI Almonertinib.Frontiers in pharmacology · 2021Article
- FOXO transcription factor family in cancer and metastasis.Cancer metastasis reviews · 2020Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundCetuximab, a monoclonal antibody against EGFR used for the treatment of colorectal cancer (CRC), is ineffective in many patients. The aim of this study was to identify the signalling pathways activated by cetuximab in CRC cells and define new biomarker of response.
methodsWe used in vitro, in vivo models and clinical CRC samples to assess the role of p38 and FOXO3a in cetuximab mechanism of action.
resultsWe show that cetuximab activates the MAPK p38. Specifically, p38 inhibition reduced cetuximab efficacy on cell growth and cell death. At the molecular level, cetuximab activates the transcription factor FOXO3a and promotes its nuclear translocation via p38-mediated phosphorylation, leading to the upregulation of its target genes p27 and BIM and the subsequent induction of apoptosis and inhibition of cell proliferation. Finally, we found that high FOXO3a and p38 expression levels are associated with better response rate and improved outcome in cetuximab-treated patients with CRC harbouring WT KRAS.
conclusionsWe identify FOXO3a as a key mediator of cetuximab mechanism of action in CRC cells and define p38 as its activator in this context. Moreover, high FOXO3a and p38 expression could predict the response to cetuximab in patients with CRC harbouring WT KRAS.
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