Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.4807
Title: The ZEB1/miR-200c feedback loop regulates invasion via actin interacting proteins MYLK and TKS5
Authors: Sundararajan, V 
Gengenbacher, N
Stemmler, M.P
Kleemann, J.A
Brabletz, T
Brabletz, S
Keywords: actin
cell protein
microRNA 200c
myosin light chain kinase
TKS5 protein
transcription factor ZEB1
unclassified drug
actin
cadherin
calcium binding protein
CDH1 protein, human
homeodomain protein
microRNA
MIRN200 microRNA, human
MYLK protein, human
myosin light chain kinase
SH3PXD2A protein, human
transcription factor
transcription factor ZEB1
vesicular transport adaptor protein
ZEB1 protein, human
actin filament
Article
breast cancer cell line
cancer control
cancer patient
cell function
computer model
controlled study
epithelial mesenchymal transition
feedback system
gene expression
genetic screening
human
human cell
protein depletion
protein determination
protein function
protein protein interaction
protein RNA binding
tumor invasion
breast tumor
cytoskeleton
female
fluorescence microscopy
gene expression regulation
HEK293 cell line
metabolism
tumor cell line
tumor invasion
Actins
Adaptor Proteins, Vesicular Transport
Breast Neoplasms
Cadherins
Calcium-Binding Proteins
Cell Line, Tumor
Cytoskeleton
Epithelial-Mesenchymal Transition
Female
Gene Expression Regulation, Neoplastic
HEK293 Cells
Homeodomain Proteins
Humans
MicroRNAs
Microscopy, Fluorescence
Myosin-Light-Chain Kinase
Neoplasm Invasiveness
Transcription Factors
Zinc Finger E-box-Binding Homeobox 1
Issue Date: 2015
Publisher: Impact Journals LLC
Citation: Sundararajan, V, Gengenbacher, N, Stemmler, M.P, Kleemann, J.A, Brabletz, T, Brabletz, S (2015). The ZEB1/miR-200c feedback loop regulates invasion via actin interacting proteins MYLK and TKS5. Oncotarget 6 (29) : 27083-27096. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.4807
Rights: Attribution 4.0 International
Abstract: Epithelial to mesenchymal transition (EMT) is a developmental process which is aberrantly activated during cancer invasion and metastasis. Elevated expression of EMTinducers like ZEB1 enables tumor cells to detach from the primary tumor and invade into the surrounding tissue. The main antagonist of ZEB1 in controlling EMT is the microRNA-200 family that is reciprocally linked to ZEB1 in a double negative feedback loop. Here, we further elucidate how the ZEB1/miR-200 feedback loop controls invasion of tumor cells. The process of EMT is attended by major changes in the actin cytoskeleton. Via in silico screening of genes encoding for actin interacting proteins, we identified two novel targets of miR-200c - TKS5 and MYLK (MLCK). Co-expression of both genes with ZEB1 was observed in several cancer cell lines as well as in breast cancer patients and correlated with low miR-200c levels. Depletion of TKS5 or MYLK in breast cancer cells reduced their invasive potential and their ability to form invadopodia. Whereas TKS5 is known to be a major component, we could identify MYLK as a novel player in invadopodia formation. In summary, TKS5 and MYLK represent two mediators of invasive behavior of cancer cells that are regulated by the ZEB1/miR-200 feedback loop.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/177758
ISSN: 19492553
DOI: 10.18632/oncotarget.4807
Rights: Attribution 4.0 International
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