Please use this identifier to cite or link to this item:
https://doi.org/10.18632/oncotarget.4807
DC Field | Value | |
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dc.title | The ZEB1/miR-200c feedback loop regulates invasion via actin interacting proteins MYLK and TKS5 | |
dc.contributor.author | Sundararajan, V | |
dc.contributor.author | Gengenbacher, N | |
dc.contributor.author | Stemmler, M.P | |
dc.contributor.author | Kleemann, J.A | |
dc.contributor.author | Brabletz, T | |
dc.contributor.author | Brabletz, S | |
dc.date.accessioned | 2020-10-20T03:15:21Z | |
dc.date.available | 2020-10-20T03:15:21Z | |
dc.date.issued | 2015 | |
dc.identifier.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 | |
dc.identifier.issn | 19492553 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/177758 | |
dc.description.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. | |
dc.publisher | Impact Journals LLC | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.source | Unpaywall 20201031 | |
dc.subject | actin | |
dc.subject | cell protein | |
dc.subject | microRNA 200c | |
dc.subject | myosin light chain kinase | |
dc.subject | TKS5 protein | |
dc.subject | transcription factor ZEB1 | |
dc.subject | unclassified drug | |
dc.subject | actin | |
dc.subject | cadherin | |
dc.subject | calcium binding protein | |
dc.subject | CDH1 protein, human | |
dc.subject | homeodomain protein | |
dc.subject | microRNA | |
dc.subject | MIRN200 microRNA, human | |
dc.subject | MYLK protein, human | |
dc.subject | myosin light chain kinase | |
dc.subject | SH3PXD2A protein, human | |
dc.subject | transcription factor | |
dc.subject | transcription factor ZEB1 | |
dc.subject | vesicular transport adaptor protein | |
dc.subject | ZEB1 protein, human | |
dc.subject | actin filament | |
dc.subject | Article | |
dc.subject | breast cancer cell line | |
dc.subject | cancer control | |
dc.subject | cancer patient | |
dc.subject | cell function | |
dc.subject | computer model | |
dc.subject | controlled study | |
dc.subject | epithelial mesenchymal transition | |
dc.subject | feedback system | |
dc.subject | gene expression | |
dc.subject | genetic screening | |
dc.subject | human | |
dc.subject | human cell | |
dc.subject | protein depletion | |
dc.subject | protein determination | |
dc.subject | protein function | |
dc.subject | protein protein interaction | |
dc.subject | protein RNA binding | |
dc.subject | tumor invasion | |
dc.subject | breast tumor | |
dc.subject | cytoskeleton | |
dc.subject | female | |
dc.subject | fluorescence microscopy | |
dc.subject | gene expression regulation | |
dc.subject | HEK293 cell line | |
dc.subject | metabolism | |
dc.subject | tumor cell line | |
dc.subject | tumor invasion | |
dc.subject | Actins | |
dc.subject | Adaptor Proteins, Vesicular Transport | |
dc.subject | Breast Neoplasms | |
dc.subject | Cadherins | |
dc.subject | Calcium-Binding Proteins | |
dc.subject | Cell Line, Tumor | |
dc.subject | Cytoskeleton | |
dc.subject | Epithelial-Mesenchymal Transition | |
dc.subject | Female | |
dc.subject | Gene Expression Regulation, Neoplastic | |
dc.subject | HEK293 Cells | |
dc.subject | Homeodomain Proteins | |
dc.subject | Humans | |
dc.subject | MicroRNAs | |
dc.subject | Microscopy, Fluorescence | |
dc.subject | Myosin-Light-Chain Kinase | |
dc.subject | Neoplasm Invasiveness | |
dc.subject | Transcription Factors | |
dc.subject | Zinc Finger E-box-Binding Homeobox 1 | |
dc.type | Article | |
dc.contributor.department | CANCER SCIENCE INSTITUTE OF SINGAPORE | |
dc.description.doi | 10.18632/oncotarget.4807 | |
dc.description.sourcetitle | Oncotarget | |
dc.description.volume | 6 | |
dc.description.issue | 29 | |
dc.description.page | 27083-27096 | |
Appears in Collections: | Staff Publications Elements |
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