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The role of the transcription factor E2F1 in hepatocellular carcinoma

FARRA, ROSSELLA
•
GRASSI, GABRIELE
•
TONON, FEDERICA
altro
DAPAS, BARBARA
2017
  • journal article

Periodico
CURRENT DRUG DELIVERY
Abstract
Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and the third leading cause of cancer-related death. Because of the fast growth, early hepatic metastasis and the multidrug resistance, the five-year survival rate is very low. Thus, the understanding of its biology can significantly contribute in identifying valuable targets for novel therapeutic approaches. In this regard, E2F1 may represent an interesting candidate. E2F1 is a transcription factor implicated in the regulation of many cellular processes including cell proliferation and apoptosis. Whereas the involvement of E2F1 in HCC has been recognized, its ability to act as a proliferative and/or apoptotic factor in HCC has not yet been clarified and, in this regard, an active debate is ongoing. The definition of E2F1 role in HCC is not a trivial aspect as it can have significant consequences for the development of novel therapeutic options with E2F1 as target. In this review, we present data about the reported proliferative/apoptotic effects as well as the dual (combined proliferation and apoptosis) functions of E2F1 in HCC discussing the molecular basis for this behavior. The data available so far indicate that the proliferative and apoptotic functions of E2F1 in HCC may coexist but the proliferative effect seems to be more pronounced than the apoptotic one.
DOI
10.2174/1567201813666160527141742
WOS
WOS:000399784000012
Archivio
http://hdl.handle.net/11368/2902433
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85013959227
http://www.eurekaselect.com/142581/article
Diritti
closed access
license:digital rights management non definito
FVG url
https://arts.units.it/request-item?handle=11368/2902433
Soggetti
  • Apoptosi

  • E2F1

  • HCC

  • miRNA

  • p53

  • Proliferation

  • Medicine (all)

  • 3003

Web of Science© citazioni
48
Data di acquisizione
Mar 23, 2024
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