Abstract
Metastasis is the main cause of cancer mortality. One of the initiating events of cancer metastasis of epithelial tumors is epithelial-to-mesenchymal transition (EMT), during which cells dedifferentiate from a relatively rigid cell structure/morphology to a flexible and changeable structure/morphology often associated with mesenchymal cells. The presence of EMT in human epithelial tumors is reflected by the increased expression of genes and levels of proteins that are preferentially present in mesenchymal cells. The combined presence of these genes forms the basis of mesenchymal gene signatures, which are the foundation for classifying a mesenchymal subtype of tumors. Indeed, tumor classification schemes that use clustering analysis of large genomic characterizations, like The Cancer Genome Atlas (TCGA), have defined mesenchymal subtype in a number of cancer types, such as high-grade serous ovarian cancer and glioblastoma. However, recent analyses have shown that gene expression-based classifications of mesenchymal subtypes often do not associate with poor survival. This “paradox” can be ameliorated using integrated analysis that combines multiple data types. We recently found that integrating mRNA and microRNA (miRNA) data revealed an integrated mesenchymal subtype that is consistently associated with poor survival in multiple cohorts of patients with serous ovarian cancer. This network consists of 8 major miRNAs and 214 mRNAs. Among the 8 miRNAs, 4 are known to be regulators of EMT. This review provides a summary of these 8 miRNAs, which were associated with the integrated mesenchymal subtype of serous ovarian cancer.
Highlights
IBWF EFGJOFE NFTFODIZNBM TVCUZQF JO B OVNCFS PG DBODFS UZQFT TVDI BT IJHI-HSBEF TFSPVT PWBSJBO DBODFS BOE HMJPCMBTUPNB )PXFWFS SFDFOU BOBMZTFT IBWF TIPXO UIBU HFOF FYQSFTTJPO-CBTFE DMBTTJGJDBUJPOT PGNFTFODIZNBMTVCUZQFTPGUFOEPOPUBTTPDJBUFXJUIQPPSTVSWJWBM5IJT “QBSBEPY”DBOCFBNFMJPSBUFE VTJOH JOUFHSBUFE BOBMZTJT UIBU DPNCJOFT NVMUJQMF EBUB UZQFT 8F SFDFOUMZ GPVOE UIBU JOUFHSBUJOH N3/" BOENJDSP3/" NJ3/"
The most well-studied cell fate switch is epithelial-to-mesenchymal transition (EMT), a process whereby epithelial cells lose both polarity and cell-to-cell contacts, acquiring increased motility and invasiveness. This pathophysiological transition is necessary for the conversion from a benign tumor to an aggressive, highly invasive carcinoma; it is the mechanism that allows tumor cells to escape from the primary tumor, evade into neighboring normal parenchyma, and enter lymphatic and blood circulation to initiate lymphohematogenous metastasis
We focus on the post-transcriptional regulatory mechanism based on microRNAs, which are 22-nucleotide, non-coding RNAs that suppress gene expression through mRNA destabilization or translational inhibition. miRNAs are deregulated in a wide variety of human cancers and have been shown to contribute to the control of cell growth, differentiation, and apoptosis, which are all important for the development and progression of cancer[18-26]. miRNAs regulate multiple signaling pathways involved in EMT[27]
Summary
IBWF EFGJOFE NFTFODIZNBM TVCUZQF JO B OVNCFS PG DBODFS UZQFT TVDI BT IJHI-HSBEF TFSPVT PWBSJBO DBODFS BOE HMJPCMBTUPNB )PXFWFS SFDFOU BOBMZTFT IBWF TIPXO UIBU HFOF FYQSFTTJPO-CBTFE DMBTTJGJDBUJPOT PGNFTFODIZNBMTVCUZQFTPGUFOEPOPUBTTPDJBUFXJUIQPPSTVSWJWBM5IJT “QBSBEPY”DBOCFBNFMJPSBUFE VTJOH JOUFHSBUFE BOBMZTJT UIBU DPNCJOFT NVMUJQMF EBUB UZQFT 8F SFDFOUMZ GPVOE UIBU JOUFHSBUJOH N3/" BOENJDSP3/" NJ3/".
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