Gα12 gep oncogene inhibits FOXO1 in hepatocellular carcinoma as a consequence of miR-135b and miR-194 dysregulation

Jung, Hye Sun; Seo, Yutaek; Yang, Yoon Mee; Koo, Ja Hyun; An, Jihyun; Lee, Seung Jin; Kim, Kang Mo; Kim, Sang Geon

doi:10.1016/j.cellsig.2014.02.022

Cited by 31 publications

(18 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…defined has-miR-429 as a key inducer for HCC pathogenesis and metastasis with potential utility for tumor intervention. Based on gene knockdown experiment, Jung et al 47. summarized that Gα12gep oncogene inhibits FOXO1 in HCC is caused by miR-135b and miR-194 dysregulation.…”

Section: Resultsmentioning

confidence: 99%

Network Consistency Projection for Human miRNA-Disease Associations Inference

Liao

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Prediction and confirmation of the presence of disease-related miRNAs is beneficial to understand disease mechanisms at the miRNA level. However, the use of experimental verification to identify disease-related miRNAs is expensive and time-consuming. Effective computational approaches used to predict miRNA-disease associations are highly specific. In this study, we develop the Network Consistency Projection for miRNA-Disease Associations (NCPMDA) method to reveal the potential associations between miRNAs and diseases. NCPMDA is a non-parametric universal network-based method that can simultaneously predict miRNA-disease associations in all diseases but does not require negative samples. NCPMDA can also confirm the presence of miRNAs in isolated diseases (diseases without any known miRNA association). Leave-one-out cross validation and case studies have shown that the predictive performance of NCPMDA is superior over that of previous method.

show abstract

Section: Resultsmentioning

confidence: 99%

Network Consistency Projection for Human miRNA-Disease Associations Inference

Liao

et al. 2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Jung and his colleagues showed that miR-135b is markedly stimulated by Gα 12 signaling in HCC cells through activator protein-1, which consistently leads to FOXO1 repression. In addition, Gα 12 QL represses miR-194 cluster gene products (194/192/215), which contributes to MDM2-mediated FOXO1 repression (Figure 2D) [77]. …”

Section: Fox-related Mirnasmentioning

confidence: 99%

MicroRNAs as regulators and mediators of forkhead box transcription factors function in human cancers

Zhang

Chen

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Evidence has shown that microRNAs are widely implicated as indispensable components of tumor suppressive and oncogenic pathways in human cancers. Thus, identification of microRNA targets and their relevant pathways will contribute to the development of microRNA-based therapeutics. The forkhead box transcription factors regulate numerous processes including cell cycle progression, metabolism, metastasis and angiogenesis, thereby facilitating tumor initiation and progression. A complex network of protein and non-coding RNAs mediates the expression and activity of forkhead box transcription factors. In this review, we summarize the current knowledge and concepts concerning the involvement of microRNAs and forkhead box transcription factors and describe the roles of microRNAs-forkhead box axis in various disease states including tumor initiation and progression. Additionally, we describe some of the technical challenges in the use of the microRNA-forkhead box signaling pathway in cancer treatment.

show abstract

“…Based on previous documents, FOXO1 acts as a tumor suppressor in HCC, the underlying molecular mechanism of the anticancer effects of FOXO1 has been widely reported as well (31)(32)(33)(34)(35). Deletion of Aurora A kinase up-regulated FOXO1 in a p53-dependent manner and induces cell cycle arrest at the G 2 /M phase (36).…”

Section: Discussionmentioning

confidence: 98%

NK3 homeobox 1 (NKX3.1) up-regulates forkhead box O1 expression in hepatocellular carcinoma and thereby suppresses tumor proliferation and invasion

Jiang

Liu

et al. 2017

Journal of Biological Chemistry

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is the leading cause of cancer-related mortality in China, and the molecular mechanism of uncontrolled HCC progression remains to be explored. NK3 homeobox 1 (), an androgen-regulated prostate-specific transcription factor, suppresses tumors in prostate cancer, but its role in HCC is unknown, especially in hepatocellular carcinoma. In the present study, the differential expression analyses in HCC tissues and matched adjacent noncancerous liver tissues revealed that NKX3.1 is frequently down-regulated in human primary HCC tissues compared with matched adjacent noncancerous liver tissues. We also noted that NKX3.1 significantly inhibits proliferation and mobility of HCC cells both and Furthermore, NKX3.1 overexpression resulted in cell cycle arrest at the G/S phase via direct binding to the promoter of forkhead box O1 () and up-regulation of expression. Of note, FOXO1 silencing in NKX3.1-overexpressing cells reversed the inhibitory effects of NKX3.1 on HCC cell proliferation and invasion. Consistently, both FOXO1 and NKX3.1 were down-regulated in human HCC tissues, and their expression was significantly and positively correlated with each other. These results suggest that functions as a tumor suppressor in HCC cells through directly up-regulating FOXO1 expression.

show abstract

Gα12 gep oncogene inhibits FOXO1 in hepatocellular carcinoma as a consequence of miR-135b and miR-194 dysregulation

Cited by 31 publications

References 39 publications

Network Consistency Projection for Human miRNA-Disease Associations Inference

Network Consistency Projection for Human miRNA-Disease Associations Inference

MicroRNAs as regulators and mediators of forkhead box transcription factors function in human cancers

NK3 homeobox 1 (NKX3.1) up-regulates forkhead box O1 expression in hepatocellular carcinoma and thereby suppresses tumor proliferation and invasion

Contact Info

Product

Resources

About