File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1038/onc.2015.371
- Scopus: eid_2-s2.0-84974589309
- PMID: 26455326
- WOS: WOS:000377474500012
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Somatic human ZBTB7A zinc finger mutations promote cancer progression
Title | Somatic human ZBTB7A zinc finger mutations promote cancer progression |
---|---|
Authors | |
Issue Date | 2016 |
Citation | Oncogene, 2016, v. 35, n. 23, p. 3071-3078 How to Cite? |
Abstract | © 2016 Macmillan Publishers Limited. We recently reported that ZBTB7A is a bona fide transcription repressor of key glycolytic genes and its downregulation in human cancer contributes to tumor metabolism. As reduced expression of ZBTB7A is found only in a subset of human cancers, we explored alternative mechanisms of its inactivation by mining human cancer genome databases. We discovered recurrent somatic mutations of ZBTB7A in multiple types of human cancers with a marked enrichment of mutations within the zinc finger domain. Functional characterization of the mutants demonstrated that mutations within the zinc finger region of ZBTB7A invariably resulted in loss of function. As a consequence, the glycolytic genes were markedly upregulated in cancer cells harboring ZBTB7A zinc finger mutation, leading to increased glycolysis and proliferation. Our study uncovers the loss-of-function mutation in ZBTB7A as a novel mechanism causing elevated glycolysis in human cancer, which carries important therapeutic implication. |
Persistent Identifier | http://hdl.handle.net/10722/260220 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 2.334 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Liu, X. S. | - |
dc.contributor.author | Liu, Z. | - |
dc.contributor.author | Gerarduzzi, C. | - |
dc.contributor.author | Choi, D. E. | - |
dc.contributor.author | Ganapathy, S. | - |
dc.contributor.author | Pandolfi, P. P. | - |
dc.contributor.author | Yuan, Z. M. | - |
dc.date.accessioned | 2018-09-12T02:00:48Z | - |
dc.date.available | 2018-09-12T02:00:48Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | Oncogene, 2016, v. 35, n. 23, p. 3071-3078 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | http://hdl.handle.net/10722/260220 | - |
dc.description.abstract | © 2016 Macmillan Publishers Limited. We recently reported that ZBTB7A is a bona fide transcription repressor of key glycolytic genes and its downregulation in human cancer contributes to tumor metabolism. As reduced expression of ZBTB7A is found only in a subset of human cancers, we explored alternative mechanisms of its inactivation by mining human cancer genome databases. We discovered recurrent somatic mutations of ZBTB7A in multiple types of human cancers with a marked enrichment of mutations within the zinc finger domain. Functional characterization of the mutants demonstrated that mutations within the zinc finger region of ZBTB7A invariably resulted in loss of function. As a consequence, the glycolytic genes were markedly upregulated in cancer cells harboring ZBTB7A zinc finger mutation, leading to increased glycolysis and proliferation. Our study uncovers the loss-of-function mutation in ZBTB7A as a novel mechanism causing elevated glycolysis in human cancer, which carries important therapeutic implication. | - |
dc.language | eng | - |
dc.relation.ispartof | Oncogene | - |
dc.title | Somatic human ZBTB7A zinc finger mutations promote cancer progression | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1038/onc.2015.371 | - |
dc.identifier.pmid | 26455326 | - |
dc.identifier.scopus | eid_2-s2.0-84974589309 | - |
dc.identifier.volume | 35 | - |
dc.identifier.issue | 23 | - |
dc.identifier.spage | 3071 | - |
dc.identifier.epage | 3078 | - |
dc.identifier.eissn | 1476-5594 | - |
dc.identifier.isi | WOS:000377474500012 | - |
dc.identifier.issnl | 0950-9232 | - |