ArticleCancer biology & therapy2014
Anti-EGFR therapeutic efficacy correlates directly with inhibition of STAT3 activity.
Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 31 citations in OpenAlex.
- A Pseudomonas aeruginosa quorum-sensing inducer controls lung permeability in establishing chronic infection via EGFR.Nature communications · 2025Article
- Shikonin suppresses colon cancer cell growth and exerts synergistic effects by regulating ADAM17 and the IL‑6/STAT3 signaling pathway.International journal of oncology · 2021Article
- Secondary resistance to anti-EGFR therapy by transcriptional reprogramming in patient-derived colorectal cancer models.Genome medicine · 2021Article
- Correlations between serum cetuximab and EGFR-related markers, and skin disorders in head and neck cancer patients.Cancer chemotherapy and pharmacology · 2021Observational
- Colorectal Cancer: From Genetic Landscape to Targeted Therapy.Journal of oncology · 2021Review
- STAT3 and p53: Dual Target for Cancer Therapy.Biomedicines · 2020Review
- STAT3 signaling in ovarian cancer: a potential therapeutic target.Journal of Cancer · 2020Review
- Signal transducer and activator of transcription-3 drives the high-fat diet-associated prostate cancer growth.Cell death & disease · 2019Article
- Drug repurposing to overcome resistance to various therapies for colorectal cancer.Cellular and molecular life sciences : CMLS · 2019Review
- Mapping the protein-protein and genetic interactions of cancer to guide precision medicine.Current opinion in genetics & development · 2019Review
- Emodin sensitizes human pancreatic cancer cells to EGFR inhibitor through suppressing Stat3 signaling pathway.Cancer management and research · 2019Article
- Ponatinib Inhibits Multiple Signaling Pathways Involved in STAT3 Signaling and Attenuates Colorectal Tumor Growth.Cancers · 2018Article
- Different responses of colorectal cancer cells to alternative sequences of cetuximab and oxaliplatin.Scientific reports · 2018Article
- Blocking of the EGFR-STAT3 signaling pathway through afatinib treatment inhibited the intrahepatic cholangiocarcinoma.Experimental and therapeutic medicine · 2018Article
- Overexpression of gelsolin reduces the proliferation and invasion of colon carcinoma cells.Molecular medicine reports · 2016Article
- Let-7a enhances the sensitivity of hepatocellular carcinoma cells to cetuximab by regulating STAT3 expression.OncoTargets and therapy · 2016Article
- MiR-20a inhibits cutaneous squamous cell carcinoma metastasis and proliferation by directly targeting LIMK1.Cancer biology & therapy · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Several agents targeting the epidermal growth factor receptor (EGFR) have been FDA-approved to treat cancer patients with varying tumor types including metastatic colorectal cancer. Many patients treated with anti-EGFR therapy however do not respond and those that do initially respond often acquire resistance. Here we show a clear correlation between the efficacy of anti-EGFR inhibitors with their ability to inhibit STAT3 activity in A431 epidermoid carcinoma cells and in a series of wt K-RAS expressing human colon cancer cell lines. Furthermore, the ability of cetuximab to inhibit growth also correlated with its ability to inhibit STAT3 activity in tumor xenograft animal studies. In addition, stable knockdown of the STAT3 phosphatase, protein tyrosine phosphatase receptor delta (PTPRD) resulted in enhanced STAT3 activity and subsequent resistance to cetuximab in DIFI colon carcinoma cells. This resistance could be reversed by STAT3 inhibition. Finally, HN5 cells with acquired resistance to the EGFR tyrosine kinase inhibitor, AG1478 displayed greater STAT3 activity than the HN5 control cell line. These AG1478-refractory HN5 cells were re-sensitized to AG1478, cetuximab and erlotinib when co-treated with a STAT3 inhibitor. Taken together, our current data indicates a key role of STAT3 activity in promoting resistance to anti-EGFR therapy and suggests that anti-EGFR therapy in combination with inhibitors that block STAT3 may provide therapeutic benefit for patients with mCRC and other EGFR driven tumor types.
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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.