PUBLICATION

Enhancement of Breast Cancer Cell Aggressiveness by lncRNA H19 and its Mir-675 Derivative: Insight into Shared and Different Actions

Authors
Peperstraete, E., Lecerf, C., Collette, J., Vennin, C., Raby, L., Völkel, P., Angrand, P.O., Winter, M., Bertucci, F., Finetti, P., Lagadec, C., Meignan, S., Bourette, R.P., Bourhis, X.L., Adriaenssens, E.
ID
ZDB-PUB-200704-2
Date
2020
Source
Cancers   12(7): (Journal)
Registered Authors
Angrand, Pierre-Olivier, Raby, Ludivine, Völkel, Pamela
Keywords
H19 gene, LncRNA, breast cancer, cancer stem cell, miR-675, tumoral progression
MeSH Terms
none
PubMed
32610610 Full text @ Cancers
Abstract
Breast cancer is a major public health problem and the leading world cause of women death by cancer. Both the recurrence and mortality of breast cancer are mainly caused by the formation of metastasis. The long non-coding RNA H19, the precursor of miR-675, is involved in breast cancer development. The aim of this work was to determine the implication but, also, the relative contribution of H19 and miR-675 to the enhancement of breast cancer metastatic potential. We showed that both H19 and miR-675 increase the invasive capacities of breast cancer cells in xenografted transgenic zebrafish models. In vitro, H19 and miR-675 enhance the cell migration and invasion, as well as colony formation. H19 seems to induce the epithelial-to-mesenchymal transition (EMT), with a decreased expression of epithelial markers and an increased expression of mesenchymal markers. Interestingly, miR-675 simultaneously increases the expression of both epithelial and mesenchymal markers, suggesting the induction of a hybrid phenotype or mesenchymal-to-epithelial transition (MET). Finally, we demonstrated for the first time that miR-675, like its precursor H19, increases the stemness properties of breast cancer cells. Altogether, our data suggest that H19 and miR-675 could enhance the aggressiveness of breast cancer cells through both common and different mechanisms.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping