ArticleOncology letters2018
EPA significantly improves anti-EGFR targeted therapy by regulating miR-378 expression in colorectal cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Prognostic model construction and drug prediction in colorectal cancer using mitochondrial programmed cell death-related genes.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Exploring The Causal Relationship Between Lipid Profiles and Colorectal Cancer Through Mendelian Randomization: A Multidimensional Plasma Lipid Composition Perspective.Journal of Cancer · 2025Article
- Correlation of Wilms' Tumor 1 (WT1) with Oxidative Stress Markers and Expression of miR-361-5p; New Aspect of WT1 in Breast Cancer.Indian journal of clinical biochemistry : IJCB · 2023Article
- Promotion or remission: a role of noncoding RNAs in colorectal cancer resistance to anti-EGFR therapy.Cell communication and signaling : CCS · 2022Review
- Article
- Krill oil supplementation reduces the growth of CT-26 orthotopic tumours in Balb/c mice.BMC complementary medicine and therapies · 2022Article
- Fish Oil and Selenium with Doxorubicin Modulates Expression of Fatty Acid Receptors and Selenoproteins, and Targets Multiple Anti-Cancer Signaling in Triple-negative Breast Cancer Tumors.International journal of medical sciences · 2022Article
- Non-Coding RNAs Regulate the Resistance to Anti-EGFR Therapy in Colorectal Cancer.Frontiers in oncology · 2021Review
- Article
- Molecular Mechanisms Associated with the Inhibitory Role of Long Chain n-3 PUFA in Colorectal Cancer.Integrative cancer therapiesReview
- Depicting the Implication of miR-378a in Cancers.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is known that colorectal cancer (CRC) cells containing mutations of the genes KRAS and BRAF are predominate mechanisms causing resistance to epidermal growth factor receptor (EGFR) inhibitors, and commonly exhibit a lower expression of microRNA-378 (miR-378) when compared with the wild type. In the present study, the aim was to determine the possible mechanism which associates miR-378 with the mitogen-activated protein kinase pathway, and to determine the efficiency of eicosapentaenoic acid ethyl ester (EPA) in its ability to restore sensitivity towards cetuximab, an EGFR inhibitor. The results demonstrated that a combined treatment of 40 µM EPA with 0.2 µM cetuximab can significantly suppress the cell growth in KRAS-mutant and control wild-type cells. Furthermore, the higher phosphorylated protein level of extracellular-signal-regulated kinase 1/2 was notable in KRAS EPA-treated cells (P=0.006-0.047) and resulted in significantly increased cell death; however, inconsistent results were indicated in EPA-treated BRAF-mutant cells, compared with the original cells (without treatment). KRAS-mutant and wild-type Caco-2 cells treated with EPA exhibited increased cetuximab response rates, but these response rates were reduced in the BRAF-mutant cells. In conclusion, upregulation of miR-378 induced by EPA may result in the significant restoration of sensitivity to cetuximab in the KRAS-mutant cells. The present data will contribute to a notable potential therapeutic solution for future clinical CRC treatments.
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