mir-31

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mir-31
Conserved secondary structure of mir-31
Identifiers
Symbolmir-31
RfamRF00661
miRBase familyMIPF0000064
Other data
RNA typemicroRNA
Domain(s)Eukaryota
PDB structuresPDBe

miR-31 has been characterised as a

tumour.[1] From its typical abundance in healthy tissue is a moderate decrease in non-metastatic breast cancer cell lines, and levels are almost completely absent in mouse and human metastatic breast cancer cell lines.[2] Mir-31-5p has also been observed upregulated in Zinc Deficient rats compared to normal in ESCC (Esophageal Squamous Cell Carcinoma) and in other types of cancers when using this animal model.[3]
There has also been observed a strong encapsulation of tumour cells expressing miR-31, as well as a reduced cell survival rate.[4] miR-31's antimetastatic effects therefore make it a potential therapeutic target for breast cancer. However, these two papers were formally retracted by the authors in 2015.

Functions

mir-31 has been linked to Duchenne muscular dystrophy − a genetic disorder characterised by a lack of the protein dystrophin − as a potential therapeutic target. Duchenne muscular dystrophy is caused by mutations arising in the dystrophin gene, which impair the translation of dystrophin through the formation of premature termination codons.[5]

miR-31 overexpression is more abundant in human Duchenne muscular dystrophy than in healthy controls, with levels remaining high only in Duchenne muscular dystrophy myoblasts. miR-31 levels in healthy controls are instead decreased with the onset of cell differentiation. miR-31 is part of the circuit controlling late muscle differentiation by repression of dystrophin synthesis, and its expression is localised specifically to regenerating myoblasts of dystrophic muscles.[6] miR-31 is believed to repress the expression of dystrophin by antisense binding of the dystrophin mRNA 3′ untranslated region, and in this way it is thought that miR-31 manipulation could aid treatment for Duchenne muscular dystrophy.

Applications

In serous ovarian cancer, miR-31 is frequently deleted and is the most underexpressed microRNA in this cancer type. It has been shown to affect the levels of gene transcription factor p53, responsible for encoding the tumour suppressor protein

gastric cancer miR-31 levels have been found to be significantly lower in tumour cells relative to healthy cells, meaning further potential for use as a diagnostic marker.[9] However, high expression levels of miR-31 correlate to shorter survival in patients with malignant pleural mesothelioma, whereas longer survival has been associated with normal/low expression of miR-31 from blood-based samples.[10]
Furthermore, in vivo, anti-miR-31 has proved to reduce miR-31-5p overexpression suppressing the esophageal preneoplasia in Zinc deficient rats. This leads to the repression of miR-31-5p target Stk40 by the inhibition of the STK40-NF-κΒ-controlled inflammatory pathway, with resultant decreased cellular proliferation and activated apoptosis. Notably Zn replenishment is able to restore the regulation of miR-31-5p targets leading to a normal esophageal phenotype.[11] miR-31 has further been shown to negatively regulate FOXP3, the master regulator in T-lymphocyte development and function.[12] This is through direct binding of miR-31 at its target site in the 3′UTR of FOXP3 mRNA.[13]

References

  1. PMID 20346098
    .
  2. PMID 19524507
    .
  3. ^ Fong LY, Taccioli C, Jing R, Smalley KJ, Alder H, Jiang Y, Fadda P, Farber JL, Croce CM (2016). "MicroRNA dysregulation and esophageal cancer development depend on the extent of zinc dietary deficiency". Oncotarget. 7 (10): 10723–38.
    PMID 26918602
    .
  4. PMID 21406558
    .
  5. PMID 21212803
    .
  6. PMID 21212803
    .
  7. S2CID 21836130
    .
  8. PMID 20179198
    .
  9. S2CID 22851497
    .
  10. PMID 26150916
    .
  11. PMID 26286729
    .
  12. PMID 19408243
    .
  13. PMID 21149603
    .

Further reading

External links


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