# Oncomir
An oncomir (also oncomiR) is a microRNA (miRNA) that acts oncogenically in cancer, typically by repressing tumor suppressor genes; the complementary class, tumor-suppressive miRNAs, inhibits oncogene expression[1](https://www.sciencedirect.com/science/article/pii/S0753332224000465). MicroRNAs are 18–25-nucleotide RNAs that do not encode proteins but control gene expression: typically they pair imperfectly with complementary sequences in the 3′-untranslated region of target transcripts, which dampens translation and destabilizes the mRNA[2](https://aacrjournals.org/cancerres/article/76/13/3666/608115/OncomiR-or-Tumor-Suppressor-The-Duplicity-of). The term was introduced by Aurora Esquela-Kerscher and Frank J. Slack in a 2006 Nature Reviews Cancer review, "Oncomirs — microRNAs with a role in cancer", after evidence showed that miRNAs can function as both tumor suppressors and oncogenes[3](https://doi.org/10.1038/NRC1840).
| Key fact | Detail |
|---|---|
| Definition | An oncogenic microRNA that promotes cancer by repressing tumor suppressor genes, through translational repression and mRNA destabilization[1](https://www.sciencedirect.com/science/article/pii/S0753332224000465) • [3](https://doi.org/10.1038/NRC1840) |
| Term coined | Esquela-Kerscher & Slack, Nature Reviews Cancer 6, 259–269 (2006)[3](https://doi.org/10.1038/NRC1840) |
| Canonical examples | miR-155, miR-21, and the miR-17∼92 cluster (also called oncomiR-1)[4](https://www.nature.com/articles/nrc3166) |
| Genomic basis | About half of annotated human miRNAs map within fragile chromosomal regions associated with various cancers[3](https://doi.org/10.1038/NRC1840) |
| Upregulation mechanisms | Transcriptional and post-transcriptional regulation, gene amplification, and tumor-microenvironment factors such as hypoxia, acidosis, and inflammation[1](https://www.sciencedirect.com/science/article/pii/S0753332224000465) • [5](https://pmc.ncbi.nlm.nih.gov/articles/PMC9523483/) |
| Therapeutic strategies | Inhibition of oncomiRs with antisense oligonucleotides (anti-miRs) and restoration of tumor-suppressive miRNAs with synthetic mimics[6](https://pubmed.ncbi.nlm.nih.gov/34088973/) |
| Research databases | OncomiR (30 cancer types, almost 10,000 TCGA patients) and the OncoMir Cancer Database (OMCD)[7](https://www.oncomir.org/oncomir/help.html) • [8](https://www.oncomir.umn.edu/omcd/basic_search.php) |
## Mechanism of action
MicroRNAs are processed from primary transcripts into mature ~18–25 nucleotide molecules that join the [RNA-induced silencing complex](https://www.edgepedia.org/rna-induced-silencing-complex) (RISC) and guide repression of complementary target mRNAs[2](https://aacrjournals.org/cancerres/article/76/13/3666/608115/OncomiR-or-Tumor-Suppressor-The-Duplicity-of). Each miRNA can control hundreds of gene targets, so a single miRNA can influence many genetic pathways at once[3](https://doi.org/10.1038/NRC1840). When an oncomiR is overexpressed, this broad repression falls on tumor suppressor and growth-control genes; conversely, loss of tumor-suppressive miRNAs enhances oncogene expression[4](https://www.nature.com/articles/nrc3166).
The miR-17-92 cluster, commonly called "oncomir-1", illustrates the effect: it targets and inhibits tumor suppressor proteins including PTEN, p21, and E2F, leading to increased cell proliferation, survival, and angiogenesis[9](https://ifccfiles.com/2025/01/eJIFCC2024vol35No4pp265-284.pdf). In mouse models, increased expression of miR-155 in the absence of other permissive mutations was sufficient to produce a malignant phenotype of lymphoid cells[10](https://farabi.university/storage/files/2654366504662f867d68a5c299636963_Dissertation_Akimniyazova_Final_Final%20%281%29.pdf), and miR-21 functions as an oncomiR in breast cancer by targeting the suppressor of cytokine signaling 1 gene (SOCS1)[11](https://pmc.ncbi.nlm.nih.gov/articles/PMC7084905/).
Cancers can become reliant on an oncomiR to an extent described as "addiction": in an in vivo model of miR-21-induced pre-[B-cell lymphoma](https://www.edgepedia.org/b-cell-lymphoma), suppressing the oncomiR resulted in complete regression of the cancer[2](https://aacrjournals.org/cancerres/article/76/13/3666/608115/OncomiR-or-Tumor-Suppressor-The-Duplicity-of).
## How oncomiR expression is dysregulated
Most mechanisms that raise oncomiR levels in cancer cells are transcriptional or post-transcriptional, but non-transcriptional processes such as gene amplification also increase oncomiR expression[1](https://www.sciencedirect.com/science/article/pii/S0753332224000465). Genomic abnormalities, including chromosomal translocations and point mutations, can stimulate or attenuate miRNA transcription; a lymphoma karyotype analysis identified a translocation containing the miR-17-92 cluster[12](https://pmc.ncbi.nlm.nih.gov/articles/PMC11159795/).
The tumor microenvironment (TME) contributes as well: hypoxia, acidosis, and inflammation are described as primary mechanisms that increase cancer-cell oncomiR expression[5](https://pmc.ncbi.nlm.nih.gov/articles/PMC9523483/). OncomiRs also participate in intercellular communication within the TME. Tumors package miRNAs into exosomes that reach immune cells; in later phases of tumor development the balance shifts toward oncomiRs produced by the tumor and miRNAs favoring immunosuppression, and exosomal miR-21-5p and miR-155-5p from macrophages have been shown to reduce the transcriptional coactivator BRG1 and enhance cancer migration and invasion[5](https://pmc.ncbi.nlm.nih.gov/articles/PMC9523483/).
## Context dependence and dual roles
The simple oncogenic-versus-suppressive classification is an oversimplification. A single miRNA can simultaneously produce competing oncogenic and tumor-suppressive effects by suppressing both tumor-suppressive mRNAs and oncogenic mRNAs, and it can also modulate extrinsic factors such as cancer-immune system interactions, stromal cell interactions, oncoviruses, and therapy sensitivity; the net effect depends on the balance of these processes[2](https://aacrjournals.org/cancerres/article/76/13/3666/608115/OncomiR-or-Tumor-Suppressor-The-Duplicity-of).
Several individual miRNAs show this duality directly. miR-7 has been described as a tumor suppressor in some cancer types and as an oncomiR in others; because it suppresses the drug efflux transporter MRP1, inhibiting miR-7 where it acts as an oncomiR could enhance chemoresistance even while slowing tumor growth[2](https://aacrjournals.org/cancerres/article/76/13/3666/608115/OncomiR-or-Tumor-Suppressor-The-Duplicity-of). miR-186 was documented as a tumor suppressor in the majority of studies, with conflicting reports verifying it as an oncomir; target abundance and dose-dependent effects help explain the contradiction[13](https://pubmed.ncbi.nlm.nih.gov/32195180/). miR-107, a member of the miR-16 family encoded within an intron of the PANK1 gene, behaves as a context-dependent "molecular switch": in tumor-suppressive settings it represses HIF-1β and cell-cycle kinases such as CDK6 and [CDK8](https://www.edgepedia.org/cdk8), while in aggressive cancers it promotes malignancy by targeting DICER1 to disrupt global miRNA biogenesis and by directly repressing PTEN, notably in bladder cancer[14](https://pubmed.ncbi.nlm.nih.gov/42230820/).
## Diagnosis and therapy
Because miRNA mis-expression correlates with cancer type and stage, miRNA expression profiling has been evaluated as a diagnostic tool; the 2006 review reported it as a more accurate method of classifying cancer subtypes than expression profiles of protein-coding genes[3](https://doi.org/10.1038/NRC1840). OncomiRs themselves are studied as clinical biomarkers and as targets for immunotherapy approaches[5](https://pmc.ncbi.nlm.nih.gov/articles/PMC9523483/).
Two therapeutic strategies follow from the biology: functional inhibition of oncogenic miRNAs with antisense oligonucleotides (anti-miRs), and replacement of tumor-suppressive miRNAs with synthetic mimics[6](https://pubmed.ncbi.nlm.nih.gov/34088973/). Delivering tumor-suppressive miRNAs and silencing oncogenic miRNAs with antagomirs has been successful in various mouse models, with delivery progressing to intranasal, intratumoral, and systemic routes[4](https://www.nature.com/articles/nrc3166).
Clinical translation has been difficult. The first miRNA mimic to reach human testing, MRX34 (a miR-34a mimic), was evaluated in a Phase I dose-escalation trial (NCT01829971) given intravenously twice weekly; of 26 patients at the maximum tolerated dose, 9 (35%) experienced grade 3/4 adverse events, and among 22 patients evaluable for RECIST response there was one partial response, 15 with stable disease, and 6 with progressive disease[15](https://molecular-cancer.biomedcentral.com/counter/pdf/10.1186/s12943-025-02298-7). The trial was withdrawn due to immune-related adverse events[16](https://www.medsci.org/v21p2781.pdf). An anti-miR-155 candidate, cobomarsen (MRG-106), a locked-nucleic-acid oligonucleotide inhibitor, entered clinical study in patients with disease progression following treatment with vorinostat[15](https://molecular-cancer.biomedcentral.com/counter/pdf/10.1186/s12943-025-02298-7).
## Research resources
Two public databases support oncomiR research. OncomiR is an online resource exploring the miRNomes of 30 cancer types, built from [The Cancer Genome Atlas](https://www.edgepedia.org/the-cancer-genome-atlas) (TCGA) with processed miRNA-Seq, RNA-Seq, and clinical data for almost 10,000 patients, and providing survival and patient-clustering analyses to identify cancer-relevant miRNAs[7](https://www.oncomir.org/oncomir/help.html). The OncoMir Cancer Database (OMCD) offers searches of miRNA statistical results based on user-defined thresholds[8](https://www.oncomir.umn.edu/omcd/basic_search.php). A noted limitation of both resources is their lack of miRNA datasets from cancer patient cohorts beyond TCGA[17](https://link.springer.com/article/10.1186/s12885-018-5085-z).
## References
1. [The regulatory mechanisms of oncomiRs in cancer, Biomedicine & Pharmacotherapy (2024)](https://www.sciencedirect.com/science/article/pii/S0753332224000465)
2. [OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer, Cancer Research (2016)](https://aacrjournals.org/cancerres/article/76/13/3666/608115/OncomiR-or-Tumor-Suppressor-The-Duplicity-of)
3. [Esquela-Kerscher, A. & Slack, F. J. Oncomirs — microRNAs with a role in cancer, Nature Reviews Cancer 6, 259–269 (2006)](https://doi.org/10.1038/NRC1840)
4. [Kasinski, A. L. & Slack, F. J. MicroRNAs en route to the clinic, Nature Reviews Cancer 11, 849–864 (2011)](https://www.nature.com/articles/nrc3166)
5. [OncomiRs as noncoding RNAs having functions in cancer: their role in immune suppression and clinical implications, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC9523483/)
6. [Cancer-associated miRNAs and their therapeutic potential, PubMed (2021)](https://pubmed.ncbi.nlm.nih.gov/34088973/)
7. [OncomiR: Help and Walkthrough](https://www.oncomir.org/oncomir/help.html)
8. [OncoMir Cancer Database (OMCD)](https://www.oncomir.umn.edu/omcd/basic_search.php)
9. [MicroRNA Significance in Cancer, eJIFCC 35(4), 265–284](https://ifccfiles.com/2025/01/eJIFCC2024vol35No4pp265-284.pdf)
10. [Dissertation citing oncomiR classification and miR-155 lymphoid malignancy models, Farabi University](https://farabi.university/storage/files/2654366504662f867d68a5c299636963_Dissertation_Akimniyazova_Final_Final%20%281%29.pdf)
11. [Regulatory Mechanism of MicroRNA Expression in Cancer, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC7084905/)
12. [The microRNA pathway and cancer, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC11159795/)
13. [The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA, PubMed (2020)](https://pubmed.ncbi.nlm.nih.gov/32195180/)
14. [The paradox of miR-107 in oncology: dual roles as a tumor suppressor and oncomiR, PubMed (2025)](https://pubmed.ncbi.nlm.nih.gov/42230820/)
15. [Table 2: miRNA-based diagnostics and therapeutics in cancer clinical trials, Molecular Cancer (2025)](https://molecular-cancer.biomedcentral.com/counter/pdf/10.1186/s12943-025-02298-7)
16. [MicroRNA in cancer therapy: breakthroughs and challenges in early clinical applications, Int. J. Med. Sci. 21, 2781 (2024)](https://www.medsci.org/v21p2781.pdf)
17. [OMCD: OncomiR Cancer Database, BMC Cancer (2018)](https://link.springer.com/article/10.1186/s12885-018-5085-z)
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*Topic: Encyclopedia › Life and health › Biological foundations › RNA and gene regulation › Small regulatory RNAs › microRNA precursor and gene families (gene records) › Cancer-associated miRNA families (oncomirs)*
*Initially written Sep 17, 2026 · Reviewed: Oct 21, 2026 · Edited: Oct 15, 2026; Oct 21, 2026 · Last review: Oct 21, 2026*
*Copyright 2026 EdgeChat AI, a subsidiary of Biostate AI.*
License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license