ArticleAmerican journal of translational research2016
Colorectal cancer cells are resistant to anti-EGFR monoclonal antibody through adapted autophagy.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- An overview of mechanisms, biomarkers, and treatment strategies for acquired anti-EGFR resistance in RAS wild-type colorectal cancer.Frontiers in pharmacology · 2025Review
- Cell Death, by Any Other Name….Cells · 2024Review
- Development ofJournal of cancer research and clinical oncology · 2023Article
- The critical role of circular RNAs in drug resistance in gastrointestinal cancers.Medical oncology (Northwood, London, England) · 2023Review
- Autophagy and the Insulin-like Growth Factor (IGF) System in Colonic Cells: Implications for Colorectal Neoplasia.International journal of molecular sciences · 2023Review
- From Intestinal Epithelial Homeostasis to Colorectal Cancer: Autophagy Regulation in Cellular Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Endocytosis at the Crossroad of Polarity and Signaling Regulation: Learning fromInternational journal of molecular sciences · 2022Review
- Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies.Journal of experimental & clinical cancer research : CR · 2021Review
- A dual-targeted molecular therapy of PP242 and cetuximab plays an anti-tumor effect through EGFR downstream signaling pathways in colorectal cancer.Journal of gastrointestinal oncology · 2021Article
- Article
- MicroRNA-216b targetsInternational journal of biological sciences · 2021Article
- Review
- Diagnostic value and prognostic significance of LI-cadherin and miR-378e in colorectal cancer.Oncology letters · 2020Article
- The Prognostic Value of Autophagy-Related Markers Bclin-1 and LC-3 in Colorectal Cancers: A Systematic Review and Meta-analysis.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Review
- The multifaceted role of autophagy in cancer and the microenvironment.Medicinal research reviews · 2019Review
- The Four Horsemen in Colon Cancer.Journal of oncology · 2019Review
- MicroRNAs in the prognosis and therapy of colorectal cancer: From bench to bedside.World journal of gastroenterology · 2018Review
- LncRNA SNHG7 sponges miR-216b to promote proliferation and liver metastasis of colorectal cancer through upregulating GALNT1.Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epidermal growth factor receptor (EGFR) signaling plays a key role in the initiation, progression, growth and metastases of colorectal carcinoma (CRC). Monoclonal antibody against EGFR (aEGFR; Cetuximab) has been used in treating CRC but some CRCs appeared to be resistant to aEGFR therapy, with undetermined mechanisms. Here, we studied the effects of aEGFR on CRC cells in vitro. We found that aEGFR dose-dependently activated Beclin-1 in 2 CRC cell lines, HT29 and SW480. Inhibition of autophagy significantly increased the aEGFR-induced CRC cell death in an CCK-8 assay. Moreover, microRNA (miR)-216b levels were significantly downregulated in aEGFR-treated CRC cells. Bioinformatics study showed that miR-216b targeted the 3'-UTR of Beclin-1 mRNA to inhibit its translation, which was confirmed by luciferase reporter assay. Together, these data suggest that aEGFR may decrease miR-216b levels in CRC cells, which subsequently upregulates Beclin-1 to increase CRC cell autophagy to antagonize aEGFR-induced cell death. Strategies that increase miR-216b levels or inhibit cell autophagy may improve the outcome of aEGFR treatment in CRC therapy.
Indexed as
Identifiers
27158405PMC4846962W2417885480What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.