mir-143

mir-143
Vertebrata
PDB structures	PDBe

In molecular biology mir-143 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. mir–143 is highly conserved in vertebrates.^[1] mir-143 is thought be involved in cardiac morphogenesis but has also been implicated in cancer.

Genomic location

mir– 143 is located on chromosome 5 position 33 in the human genome.

Their co-transcription means they are frequently studied together in the same cellular pathways and diseases.

Expression

mir–143 is a direct transcriptional target of the serum response factor, myocardin and nkx2-5.[2] mir-143 expression is also thought to be controlled epigenetically through heart beat.^[3]

Targets

These are known genetic targets for mir–143 and its effect on them:

• Klf4 – Promotes transcription.^[2]
• ELK1 – Promotes transcription.^[2]
• ADD3 – Represses transcription. F-actin capping protein.^[4]
• FNDC38 – Represses transcription. Tumour metastasis.^[5]
• HK2 – Represses transcription. Glucose-6-phosphate catalyzing enzyme.^[6]
• Raldh2/aldh1a2 – Represses transcription. Involved in heart tube organization.^[3]
• rxrab – Represses transcription. Involved in heart tube organization.^[3]
• KLF5 – Unknown has conserved miR – 143 binding site.^[1]
• MAP3K7– Unknown has conserved miR – 143 binding site.^[1]
• TARDBP – Unknown has conserved miR – 143 binding site.^[1]
• UBE2E3– Unknown has conserved miR – 143 binding site.^[1]

Cardiogenesis

mir-143 is thought to play an important role in cardiac morphogenesis. mir–143 was found to be the most enriched miRNA in mouse embryonic stem cells that were differentiating into cardiac progenitor cells.

MiR-143 has also been implicated in the more general morphogenesis of the heart. In zebrafish it was shown that mir-143 is required for chamber morphogenesis through repression of add3. A knockout resulted in ventricular collapse.[4] It has also been suggested that mir-143 expression may be controlled by heart beat. In zebrafish mir-143 expression was absent when heartbeat was arrested and restored when heartbeat was reinitiated.^[3] Understanding mir– 143 may be important for understanding vascular disease. The plasticity of VSMCs is thought to be the basis of many human vascular diseases such as atherosclerosis.^[7] It has also been shown that in human aortic aneurysms the expression of mir-143 and mir-145 were found to be significantly decreased when compared to controls.^[8]

Cancer

Changes in mir-143 expression have frequently been implicated in cancer. However the exact nature of this relationship is not fully understood. The up-regulation of mir-143 was observed in a hepatocellular carcinoma model during tumor

References

Further reading

• Kulda V, Pesta M, Topolcan O, et al. (2010). "Relevance of miR-21 and miR-143 expression in tissue samples of colorectal carcinoma and its liver metastases". Cancer Genet Cytogenet. 200 (2): 154–60.
  PMID 20620599
  .
• Yang Y, Chaerkady R, Kandasamy K, et al. (2010). "Identifying targets of miR-143 using a SILAC-based proteomic approach". Mol Biosyst. 6 (10): 1873–82.
  PMID 20544124
  .
• Iio A, Nakagawa Y, Hirata I, et al. (2010). "Identification of non-coding RNAs embracing microRNA-143/145 cluster". Mol Cancer. 9: 136.
  PMID 20525177
  .
• Wang X, Hu G, Zhou J (2010). "Repression of versican expression by microRNA-143". J Biol Chem. 285 (30): 23241–50.
  PMID 20489207
  .
• Gao W, Yu Y, Cao H, et al. (2010). "Deregulated expression of miR-21, miR-143 and miR-181a in non-small cell lung cancer is related to clinicopathologic characteristics or patient prognosis". Biomed Pharmacother. 64 (6): 399–408.
  PMID 20363096
  .
• Akao Y, Nakagawa Y, Hirata I, et al. (2010). "Role of anti-oncomirs miR-143 and -145 in human colorectal tumors". Cancer Gene Ther. 17 (6): 398–408.
  S2CID 27389187
  .
• Clapé C, Fritz V, Henriquet C, et al. (2009). Creighton C (ed.). "miR-143 interferes with ERK5 signaling, and abrogates prostate cancer progression in mice". PLOS ONE. 4 (10): e7542.
  PMID 19855844
  .
• Borralho PM, Kren BT, Castro RE, et al. (2009). "MicroRNA-143 reduces viability and increases sensitivity to 5-fluorouracil in HCT116 human colorectal cancer cells". FEBS J. 276 (22): 6689–700.
  S2CID 205881537
  .
• Xin M, Small EM, Sutherland LB, et al. (2009). "MicroRNAs miR-143 and miR-145 modulate cytoskeletal dynamics and responsiveness of smooth muscle cells to injury". Genes Dev. 23 (18): 2166–78.
  PMID 19720868
  .
• Zhang R, Wang L, Yang AG (2009). "Is microRNA-143 really a turncoat of tumor suppressor microRNA in hepatitis B virus-related hepatocellular carcinoma?". Hepatology. 50 (3): 987, author reply 987–8.
  S2CID 2177122
  .
• Ng EK, Tsang WP, Ng SS, et al. (2009). "MicroRNA-143 targets DNA methyltransferases 3A in colorectal cancer". Br J Cancer. 101 (4): 699–706.
  PMID 19638978
  .
• Zhang X, Liu S, Hu T, et al. (2009). "Up-regulated microRNA-143 transcribed by nuclear factor kappa B enhances hepatocarcinoma metastasis by repressing fibronectin expression". Hepatology. 50 (2): 490–9.
  S2CID 32196346
  .
• Akao Y, Nakagawa Y, Iio A, et al. (2009). "Role of microRNA-143 in Fas-mediated apoptosis in human T-cell leukemia Jurkat cells". Leuk Res. 33 (11): 1530–8.
  PMID 19464056
  .

External links

• Page for mir-143 microRNA precursor family at Rfam