ArticleOncotarget2016
miR-143 or miR-145 overexpression increases cetuximab-mediated antibody-dependent cellular cytotoxicity in human colon cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 51 citations in OpenAlex.
- Data on microRNA transcriptomic signatures, predicted gene targets and pathway analysis in response to cetuximab or panitumumab in colorectal cancer cells.Data in brief · 2026Article
- Co-expression of miRNA players in advanced laryngeal carcinoma - Insights into the roles of miR-93-5p, miR-145-5p, and miR-210-3p.Biomolecules & biomedicine · 2025Article
- Targeting microRNA-143 in colorectal cancer: advances in molecular biosciences for biomarker-based diagnostics, therapeutic strategies, and drug resistance prediction.Frontiers in molecular biosciences · 2025Review
- Statins and their impact on epigenetic regulation: insights into disease.Frontiers in pharmacology · 2025Review
- Unraveling the Regulatory Role of HuR/microRNA Axis in Colorectal Cancer Tumorigenesis.Cancers · 2024Review
- Strong YKL-40 expression in the invasive tumor front of colorectal cancer-A pilot study.Heliyon · 2024Article
- miR-373 promotes invasion and metastasis of colorectal cancer cells via activating ERK/MAPK pathway.Scientific reports · 2024Article
- Cooperatively inhibition effect of miR-143-5p and miR-145-5p in tumorigenesis of glioblastoma cells through modulating AKT signaling pathway.BioImpacts : BI · 2024Article
- Article
- Review
- Promotion or remission: a role of noncoding RNAs in colorectal cancer resistance to anti-EGFR therapy.Cell communication and signaling : CCS · 2022Review
- Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer.Biomolecules · 2021Review
- Review
- Non-Coding RNAs Regulate the Resistance to Anti-EGFR Therapy in Colorectal Cancer.Frontiers in oncology · 2021Review
- MiR-145 in cancer therapy resistance and sensitivity: A comprehensive review.Cancer science · 2020Review
- Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview.Cancer science · 2020Review
- c-MYC Expression Is a Possible Keystone in the Colorectal Cancer Resistance to EGFR Inhibitors.Cancers · 2020Article
- MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients.Non-coding RNA · 2020Review
- LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143.Cancer management and research · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
miR-143 and miR-145 are downregulated in colon cancer. Here, we tested the effect of restoring these miRNAs on sensitization to cetuximab in mutant KRAS (HCT116 and SW480) and wild-type KRAS (SW48) colon cancer cells. We evaluated cetuximab-mediated antibody-dependent cellular cytotoxicity (ADCC) and the modulation of signaling pathways involved in immune effector cell-mediated elimination of cancer cells. Stable miR-143 or miR-145 overexpression increased cell sensitivity to cetuximab, resulting in a significant increase of cetuximab-mediated ADCC independently of KRAS status. Importantly, HCT116 cells overexpressing these miRNAs triggered apoptosis in result of cetuximab-mediated ADCC, effected by peripheral blood mononuclear cells (p < 0.01). This was associated with increased apoptosis and caspase-3/7 activity, and reduced Bcl-2 protein expression (p < 0.01). In addition, caspase inhibition abrogated cetuximab-mediated ADCC in HCT116 cells overexpressing either miR-143 or miR-145 (p < 0.01). Furthermore, Bcl-2 silencing led to high level of cetuximab-mediated ADCC, compared to control siRNA (p < 0.05). Importantly, granzyme B inhibition, abrogated cetuximab-mediated ADCC, reducing caspase-3/7 activity (p < 0.01). Collectively, our data suggests that re-introduction of miR-143 or miR-145 may provide a new approach for development of therapeutic strategies to re-sensitize colon cancer cells to cetuximab by stimulating cetuximab-dependent ADCC to induce cell death.
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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.