dc.contributor.author | Valeri, N | |
dc.contributor.author | Braconi, C | |
dc.contributor.author | Gasparini, P | |
dc.contributor.author | Murgia, C | |
dc.contributor.author | Lampis, A | |
dc.contributor.author | Paulus-Hock, V | |
dc.contributor.author | Hart, JR | |
dc.contributor.author | Ueno, L | |
dc.contributor.author | Grivennikov, SI | |
dc.contributor.author | Lovat, F | |
dc.contributor.author | Paone, A | |
dc.contributor.author | Cascione, L | |
dc.contributor.author | Sumani, KM | |
dc.contributor.author | Veronese, A | |
dc.contributor.author | Fabbri, M | |
dc.contributor.author | Carasi, S | |
dc.contributor.author | Alder, H | |
dc.contributor.author | Lanza, G | |
dc.contributor.author | Gafa', R | |
dc.contributor.author | Moyer, MP | |
dc.contributor.author | Ridgway, RA | |
dc.contributor.author | Cordero, J | |
dc.contributor.author | Nuovo, GJ | |
dc.contributor.author | Frankel, WL | |
dc.contributor.author | Rugge, M | |
dc.contributor.author | Fassan, M | |
dc.contributor.author | Groden, J | |
dc.contributor.author | Vogt, PK | |
dc.contributor.author | Karin, M | |
dc.contributor.author | Sansom, OJ | |
dc.contributor.author | Croce, CM | |
dc.date.accessioned | 2020-08-14T15:39:47Z | |
dc.date.issued | 2014-04-14 | |
dc.identifier.citation | Cancer cell, 2014, 25 (4), pp. 469 - 483 | |
dc.identifier.issn | 1535-6108 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/3973 | |
dc.identifier.eissn | 1878-3686 | |
dc.identifier.doi | 10.1016/j.ccr.2014.03.006 | |
dc.description.abstract | MicroRNA deregulation is frequent in human colorectal cancers (CRCs), but little is known as to whether it represents a bystander event or actually drives tumor progression in vivo. We show that miR-135b overexpression is triggered in mice and humans by APC loss, PTEN/PI3K pathway deregulation, and SRC overexpression and promotes tumor transformation and progression. We show that miR-135b upregulation is common in sporadic and inflammatory bowel disease-associated human CRCs and correlates with tumor stage and poor clinical outcome. Inhibition of miR-135b in CRC mouse models reduces tumor growth by controlling genes involved in proliferation, invasion, and apoptosis. We identify miR-135b as a key downsteam effector of oncogenic pathways and a potential target for CRC treatment. | |
dc.format | Print | |
dc.format.extent | 469 - 483 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | CELL PRESS | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0 | |
dc.subject | Cell Line, Tumor | |
dc.subject | Animals | |
dc.subject | Mice, Inbred C57BL | |
dc.subject | Humans | |
dc.subject | Mice | |
dc.subject | Mice, Nude | |
dc.subject | Colonic Neoplasms | |
dc.subject | Disease Models, Animal | |
dc.subject | Disease Progression | |
dc.subject | MicroRNAs | |
dc.subject | Immunohistochemistry | |
dc.subject | Transfection | |
dc.subject | Cell Growth Processes | |
dc.subject | Heterografts | |
dc.title | MicroRNA-135b promotes cancer progression by acting as a downstream effector of oncogenic pathways in colon cancer. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2014-03-06 | |
rioxxterms.versionofrecord | 10.1016/j.ccr.2014.03.006 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by-nc-nd/4.0 | |
rioxxterms.licenseref.startdate | 2014-04 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Cancer cell | |
pubs.issue | 4 | |
pubs.notes | Not known | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Signal Transduction & Molecular Pharmacology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Evolutionary Genomics & Modelling | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Gastrointestinal Cancer Biology and Genomics | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Signal Transduction & Molecular Pharmacology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Evolutionary Genomics & Modelling | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Gastrointestinal Cancer Biology and Genomics | |
pubs.publication-status | Published | |
pubs.volume | 25 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Signal Transduction & Molecular Pharmacology | |
icr.researchteam | Evolutionary Genomics & Modelling | |
icr.researchteam | Gastrointestinal Cancer Biology and Genomics | |
dc.contributor.icrauthor | Valeri, Nicola | |
dc.contributor.icrauthor | Braconi, Chiara | |
dc.contributor.icrauthor | Lampis, Andrea | |