Mir-22

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Precursor microRNA family

title: "Mir-22" type: doc version: 1 created: 2026-02-28 author: "Wikipedia contributors" status: active scope: public tags: ["microrna"] description: "Precursor microRNA family" topic_path: "general/microrna" source: "https://en.wikipedia.org/wiki/Mir-22" license: "CC BY-SA 4.0" wikipedia_page_id: 0 wikipedia_revision_id: 0

::summary Precursor microRNA family ::

::data[format=table title="Infobox rfam"]

Field	Value
Name	mir-22
image	MiR-22 secondary structure.png
caption	miR-22 microRNA secondary structure and sequence conservation
Symbol	mir-22
Rfam	RF00653
miRBase_family	MIPF0000053
RNA_type	microRNA
Tax_domain	Eukaryota; Euteleostomi
EntrezGene	407004
HGNCid	31599
OMIM	612077
::

In molecular biology mir-22 microRNA is a short RNA molecule. MicroRNAs are an abundant class of molecules, approximately 22 nucleotides in length, which can post-transcriptionally regulate gene expression by binding to the 3' UTR of mRNAs expressed in a cell.

Origins

Mir-22 was originally identified in HeLa cells (an immortal cell line derived from cervical cancer cells), but was later found to be ubiquitously expressed in various tissues. The gene encoding miR-22 is found on the short arm of chromosome 17, in a minimal loss of heterozygosity region. It is highly conserved across many vertebrate species, including chimp, mouse, rat, dog and horse. This level of conservation suggests functional importance. MiR-22 was previously identified as having a role in erythrocyte maturation.

Role in cancer

The deregulation of many miRNAs has been shown to have a role in oncogenesis. Mir-22 was found to be over-expressed in prostate cancer but down-regulated in breast cancer, cholangiocarcinoma, multiple myeloma and hepatocellular carcinoma. Mir-22 expression was associated with survival in multiple breast cancer datasets.

Targets

Specifically, miR-22 can function as a tumour suppressor. One known target is histone deacetylase 4 (HDAC4), which is known to have a critical role in cancer development. Mir-22 also targets Myc Binding Protein (MYCBP). This prevents transcription of c-Myc target genes by silencing c-MYCBP. However, c-Myc also inhibits expression of miR-22 in a positive feedback loop. When this spirals out of control, it can cause uncontrolled cell proliferation.

Possible therapy

Expression of miR-22 can be induced by adding 12-O-Tetradecanoylphorbol-13-acetate (TPA) to HL-60 cells (leukaemia cell line). The enforced expression causes the growth of cancer cells to slow down. This means that miR-22 could be a potential target for cancer therapies.

References

(2010). "An estrogen receptor alpha suppressor, microRNA-22, is downregulated in estrogen receptor alpha-positive human breast cancer cell lines and clinical samples.". FEBS J.
(April 2007). "MicroRNA expression profiling during human cord blood-derived CD34 cell erythropoiesis". Exp. Hematol..
(2010). "microRNA-22, downregulated in hepatocellular carcinoma and correlated with prognosis, suppresses cell proliferation and tumourigenicity". Br J Cancer.
(2016-12-01). "miRpower: a web-tool to validate survival-associated miRNAs utilizing expression data from 2178 breast cancer patients". Breast Cancer Research and Treatment.
(2010). "Tumor-suppressive microRNA-22 inhibits the transcription of E-box-containing c-Myc target genes by silencing c-Myc binding protein". Oncogene.
(May 1999). "The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation". Oncogene.
(2010). "Differentiation-associated miR-22 represses Max expression and inhibits cell cycle progression". Biochem Biophys Res Commun.

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