TY - JOUR
T1 - Post-transcriptional regulatory network of epithelial-to-mesenchymal and mesenchymal-to-epithelial transitions
AU - Guo, Fei
AU - Parker Kerrigan, Brittany C.
AU - Yang, Da
AU - Hu, Limei
AU - Shmulevich, Ilya
AU - Sood, Anil K.
AU - Xue, Fengxia
AU - Zhang, Wei
N1 - Funding Information:
We thank Ms. Ann Sutton in the Department of Scientific Publications at MD Anderson for editing this manuscript. This study was partially supported by U.S. National Institutes of Health grants U24 CA143835, P50 CA083639, and U54 CA151668; MD Anderson support grant CA016672; and a grant from the Blanton-Davis Ovarian Cancer Research Program.
PY - 2014/3/5
Y1 - 2014/3/5
N2 - Epithelial-to-mesenchymal transition (EMT) and its reverse process, mesenchymal-to-epithelial transition (MET), play important roles in embryogenesis, stem cell biology, and cancer progression. EMT can be regulated by many signaling pathways and regulatory transcriptional networks. Furthermore, post-transcriptional regulatory networks regulate EMT; these networks include the long non-coding RNA (lncRNA) and microRNA (miRNA) families. Specifically, the miR-200 family, miR-101, miR-506, and several lncRNAs have been found to regulate EMT. Recent studies have illustrated that several lncRNAs are overexpressed in various cancers and that they can promote tumor metastasis by inducing EMT. MiRNA controls EMT by regulating EMT transcription factors or other EMT regulators, suggesting that lncRNAs and miRNA are novel therapeutic targets for the treatment of cancer. Further efforts have shown that non-coding-mediated EMT regulation is closely associated with epigenetic regulation through promoter methylation (e.g., miR-200 or miR-506) and protein regulation (e.g., SET8 via miR-502). The formation of gene fusions has also been found to promote EMT in prostate cancer. In this review, we discuss the post-transcriptional regulatory network that is involved in EMT and MET and how targeting EMT and MET may provide effective therapeutics for human disease.
AB - Epithelial-to-mesenchymal transition (EMT) and its reverse process, mesenchymal-to-epithelial transition (MET), play important roles in embryogenesis, stem cell biology, and cancer progression. EMT can be regulated by many signaling pathways and regulatory transcriptional networks. Furthermore, post-transcriptional regulatory networks regulate EMT; these networks include the long non-coding RNA (lncRNA) and microRNA (miRNA) families. Specifically, the miR-200 family, miR-101, miR-506, and several lncRNAs have been found to regulate EMT. Recent studies have illustrated that several lncRNAs are overexpressed in various cancers and that they can promote tumor metastasis by inducing EMT. MiRNA controls EMT by regulating EMT transcription factors or other EMT regulators, suggesting that lncRNAs and miRNA are novel therapeutic targets for the treatment of cancer. Further efforts have shown that non-coding-mediated EMT regulation is closely associated with epigenetic regulation through promoter methylation (e.g., miR-200 or miR-506) and protein regulation (e.g., SET8 via miR-502). The formation of gene fusions has also been found to promote EMT in prostate cancer. In this review, we discuss the post-transcriptional regulatory network that is involved in EMT and MET and how targeting EMT and MET may provide effective therapeutics for human disease.
KW - Epithelial-to-mesenchymal transition (EMT)
KW - Long non-coding RNA (lncRNA)
KW - Mesenchymal-to-epithelial transition (MET)
KW - microRNA (miRNA)
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U2 - 10.1186/1756-8722-7-19
DO - 10.1186/1756-8722-7-19
M3 - Review article
C2 - 24598126
AN - SCOPUS:84898030144
SN - 1756-8722
VL - 7
JO - Journal of Hematology and Oncology
JF - Journal of Hematology and Oncology
IS - 1
M1 - 19
ER -