MicroRNAs in the etiology of colorectal cancer: Pathways and clinical implications
Open accessAbstract
MicroRNAs (miRNAs) are small single-stranded RNAs that repress mRNA translation and trigger mRNA degradation. Of the ∼1900 miRNA-encoding genes present in the human genome, ∼250 miRNAs are reported to have changes in abundance or altered functions in colorectal cancer. Thousands of studies have documented aberrant miRNA levels in colorectal cancer, with some miRNAs reported to actively regulate tumorigenesis. A recurrent phenomenon with miRNAs is their frequent participation in feedback loops, which probably serve to reinforce or magnify biological outcomes to manifest a particular cellular phenotype. Here, we review the roles of oncogenic miRNAs (oncomiRs), tumor suppressive miRNAs (anti-oncomiRs) and miRNA regulators in colorectal cancer. Given their stability in patient-derived samples and ease of detection with standard and novel techniques, we also discuss the potential use of miRNAs as biomarkers in the diagnosis of colorectal cancer and as prognostic indicators of this disease. MiRNAs also represent attractive candidates for targeted therapies because their function can be manipulated through the use of synthetic antagonists and miRNA mimics.
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Certain miRNAs can regulate expression of target genes that are involved in drug response pathways, e.g., TP53, BCL2 (apoptosis) and KRAS, PTEN (cell proliferation and survival).
“For instance, certain miRNAs can regulate expression of target genes that are involved in drug response pathways, e.g., TP53, BCL2 (apoptosis) and KRAS, PTEN (cell proliferation and survival) [61].”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [61]
The sections on TP53, KRAS and miR-21/miR-221 describe miRNA regulation of TP53 levels, KRAS activity and PTEN, and the Introduction links KRAS mutations to resistance to EGFR inhibitors (page numbers unavailable). The miR-21 section reports altered BCL2 levels when miR-21 is lost, but does not establish BCL2 as a miRNA target; nor does the review link all four named genes to drug response pathways as the sentence implies. (LLM, conf=0.85)
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References 320 · Cited by 147
- Authors
- Strubberg, A. M., & Madison, B. B.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Madison, Blair B.
- ORCID
- Madison, Blair B.
- Venue
- Disease Models & Mechanisms
- Publisher
- The Company of Biologists
- Published
- 2017-03-01
- Volume
- 10
- Issue
- 3
- Pages
- 197-214
- ISSN
- 1754-8403 (ISSN-L)
- 1754-8411
- PMC
- PMC5374322
- OpenAlex
- W2594158458
- Cited by
- 147
- References
- 320
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 12 · 2023: 17 · 2022: 19 · 2021: 21 · 2020: 23 · 2019: 23 · 2018: 11 · 2017: 4
- FWCI
- 1.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Disease Models & Mechanisms (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (K01-DK093885, 1R03-DK108764, P30-DK052574)
- Siteman Cancer Center
- Cancer Research Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Plant Molecular Biology Research
- Keywords
- microRNA, colorectal cancer, oncogenic microRNA, tumor suppressor microRNA, feedback loops, carcinogenesis, tumor markers, prognostic factors, miRNA mimics, miRNA inhibitors
- MeSH terms
- Animals, Humans, Neoplastic Stem Cells, Colorectal Neoplasms, Signal Transduction, MicroRNAs, Genetic Pleiotropy, Carcinogenesis
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