Epithelial-Mesenchymal Transition  is the process by which epithelial cells lose cell-cell junctions and baso-apical polarity while acquire plasticity, mobility, invasive capacity, stem-like characteristics, and apoptosis resistance. The cellular program is normally active in embryogenesis and wound healing. Pathologically EMT is also active in cancer metastasis which provides critical impetus for epithelial malignancies to acquire metastatic capability . Recent research has suggested that LncRNAs might be key regulators of EMT process, adding an important new layer to our understanding of tumor cell plasticity and the regulation of EMT pathway in cancers.
The LncPath™ Human EMT Pathway LncRNA Microarray simultaneously profiles the expression of 773 LncRNAs and 219 their potential coding targets related to EMT signaling pathway. The LncPath™ Mouse EMT Pathway LncRNA Microarray simultaneously profiles the expression of 386 LncRNAs and 357 their potential coding targets related to EMT signaling pathway. All the LncRNAs that have already been proven to be associated with the EMT pathway are manually curated from literature. Furthermore, the LncRNAs whose gene loci located at or near the protein-coding genes critical in EMT pathway, and the LncRNAs which have high possibility as the potential ceRNAs of the key EMT-associated genes, are also carefully selected from the authoritative databases by using a rigorous process. By limiting LncRNAs to those most relevant to EMT pathway, analysis can be achieved quickly and precisely due to a highly specific yet smaller data set. The expressional relationship between the EMT-associated LncRNAs and their potential protein-coding targets can be established to gain comprehensive insights into the underlying regulatory mechanisms of LncRNAs in EMT process.
• Reliable EMT pathway focus LncRNA collection
• Simultaneous analysis of LncRNAs and their potential coding gene targets related to the EMT pathway
• Efficient and robust labeling system
• Innovative probe design
• Guaranteed performance
An example showing the detailed information about the LncRNAs and their potential coding gene target
Click the LncRNA accession number listed in databases, you will see the figures showing the detailed information about the LncRNAs and their potential target gene.
Figure 1. The genomic map views of , the LncRNA ENST00000557223 and its potential target gene AKT1. From the top to the bottom of the figure 1, the following items are displayed:
Genome view: A chromosome ideogram showing the map position of the LncRNA ENST00000557223 and its potential target gene AKT1 (red bar).
Map view ruler: The map coordinates of the human genome assembly hg19 for the map views below.
LncRNA map view: The LncRNAs whose genes located at or near the AKT1 gene are presented in the Noncoding panel (shaded green). The LncRNAs are indicated by the transcript IDs, the exons by solid blocks, the introns by thin lines, and the transcription directions by arrows. The exons of LncRNA ENST00000557223 are labeled in red, while the exons of the other LncRNAs are labeled in blue.
Coding gene map view: The coding gene AKT1 is presented in the Coding panel (shaded blue). The coding gene is indicated by its canonical transcript ID, the exons by solid blocks, the introns by thin lines, and the transcription direction by arrows.
Figure 2. The relationship between LncRNA ENST00000557223 and its protein coding gene target AKT1. The other neighboring LncRNAs which may regulate AKT1 expression are also shown.
Figure 3. The LncRNA uc010mzx.1 may function as a competing endogenous RNA (ceRNA) of the protein coding gene AKT1.
* MuTaMe Score, Mutually Targeted MRE Enrichment Score .
References1. Nordentoft, I., et al., miRNAs associated with chemo-sensitivity in cell lines and in advanced bladder cancer. BMC Med Genomics, 2012. 5(1): p. 40.
2. Talbot, L.J., S.D. Bhattacharya, and P.C. Kuo, Epithelial-mesenchymal transition, the tumor microenvironment, and metastatic behavior of epithelial malignancies. Int J Biochem Mol Biol, 2012. 3(2): p. 117-36.
3. Tay, Y., et al., Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs. Cell, 2011. 147(2): p. 344-57.