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2015 ; 14
(ä): 87
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The role of the PI3K/Akt/mTOR signalling pathway in human cancers induced by
infection with human papillomaviruses
#MMPMID26022660
Zhang L
; Wu J
; Ling MT
; Zhao L
; Zhao KN
Mol Cancer
2015[Apr]; 14
(ä): 87
PMID26022660
show ga
Infection with Human papillomaviruses (HPVs) leads to the development of a
wide-range of cancers, accounting for 5% of all human cancers. A prominent
example is cervical cancer, one of the leading causes of cancer death in women
worldwide. It has been well established that tumor development and progression
induced by HPV infection is driven by the sustained expression of two oncogenes
E6 and E7. The expression of E6 and E7 not only inhibits the tumor suppressors
p53 and Rb, but also alters additional signalling pathways that may be equally
important for transformation. Among these pathways, the phosphatidylinositol
3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signalling cascade plays
a very important role in HPV-induced carcinogenesis by acting through multiple
cellular and molecular events. In this review, we summarize the frequent
amplification of PI3K/Akt/mTOR signals in HPV-induced cancers and discuss how HPV
oncogenes E6/E7/E5 activate the PI3K/Akt/mTOR signalling pathway to modulate
tumor initiation and progression and affect patient outcome. Improvement of our
understanding of the mechanism by which the PI3K/Akt/mTOR signalling pathway
contributes to the immortalization and carcinogenesis of HPV-transduced cells
will assist in devising novel strategies for preventing and treating HPV-induced
cancers.