2017
DOI: 10.1002/hep.29183
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Amplification and/or activation of the c-Myc protooncogene is one of the leading genetic events along hepatocarcinogenesis. The oncogenic potential of c-Myc has been proven experimentally by the finding that its overexpression in the mouse liver triggers tumor formation. However, the molecular mechanism whereby c-Myc exerts its oncogenic activity in the liver remains poorly understood. Here, we demonstrate that the mammalian target of rapamycin complex 1 (mTORC1) cascade is activated and necessary for c-Myc de… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

4
149
0

Year Published

2018
2018
2023
2023

Publication Types

Select...
7

Relationship

1
6

Authors

Journals

citations
Cited by 126 publications
(153 citation statements)
references
References 45 publications
4
149
0
Order By: Relevance
“…Hyperactive AKT‐mTOR signaling is a common phenomenon in HCC . Activation of AKT and mTOR is critical for HCG in various common HCC models in mice . However, a recent clinical trial did not achieve desirable endpoints on the rapamycin analog, everolimus, in advanced HCC patients .…”
mentioning
confidence: 99%
See 1 more Smart Citation
“…Hyperactive AKT‐mTOR signaling is a common phenomenon in HCC . Activation of AKT and mTOR is critical for HCG in various common HCC models in mice . However, a recent clinical trial did not achieve desirable endpoints on the rapamycin analog, everolimus, in advanced HCC patients .…”
mentioning
confidence: 99%
“…(20,21) Activation of AKT and mTOR is critical for HCG in various common HCC models in mice. (22)(23)(24)(25) However, a recent clinical trial did not achieve desirable endpoints on the rapamycin analog, everolimus, in advanced HCC patients. (26,27) Therefore, identifying new treatment strategies, such as combination therapy, is necessary for improving the efficacy of rapamycin and rapamycin analogs in order to bring mTOR-targeted therapies into the clinic.…”
mentioning
confidence: 99%
“…Activation of the mTORC1 cascade was essential for c‐Myc‐dependent hepatocarcinogenesis. Ablation of RAPTOR strongly inhibited c‐Myc liver tumor formation via quenching mTORC1 cascades and downregulating SLC1A5 and SLC7A6, which further weakened mTORC1 . LncRNA MALAT1 contributed to HCC development by enhancing the translation of the metabolic transcription factor TCF7L2.…”
Section: Discussionmentioning
confidence: 99%
“…2,3 Increasing reports have shown that mTORC1 is frequently activated in various cancers, particularly in digestive malignant tumors, such as colorectal cancer (CRC), 4 gastric cancer, 5 pancreatic ductal adenocarcinoma (PDAC), 6 and hepatocellular carcinoma (HCC). 7 Although the activity of mTORC1 can be counteracted by the clinical inhibitor, everolimus, there still exists a formidable obstacle of extensive clinical application due to resistance resulting from the limitation of everolimus on the mTORC1 cascade and complex tumor microenvironment. [8][9][10] Therefore, exploring mTORC1 signaling is an urgent priority since its exploitation may remedy the therapeutic limitations of rapamycin analogues.…”
Section: Introductionmentioning
confidence: 99%
“…Thus, Bclaf1 is a bona fide Hsp90α client and provides one rational for the addiction of HCC to Hsp90α. ( ) Interaction of Bclaf1 with Hsp90α depends on Hsp90’s C‐terminal domain and is prevented by an Hsp90 inhibitor that binds to the C‐terminal domain, NB, but not a nucleotide competitive inhibitor, providing one explanation for the antitumor growth effect of NB.…”
Section: Discussionmentioning
confidence: 99%