| Title |
HIF-2α regulates CDCP1 to promote PKCδ-mediated migration in hepatocellular carcinoma
|
|---|---|
| Published in |
Tumor Biology, August 2015
|
| DOI | 10.1007/s13277-015-3527-7 |
| Pubmed ID | |
| Authors |
Manqing Cao, Junrong Gao, Hongyuan Zhou, Jiafei Huang, Abin You, Zhigui Guo, Feng Fang, Wei Zhang, Tianqiang Song, Ti Zhang |
| Abstract |
Overexpression of CUB domain-containing protein 1 (CDCP1), a transmembrane glycoprotein and major substrate of Src family kinases (SFKs), always indicates unfavorable outcomes in various cancers. The characteristics of CDCP1 in hepatocellular carcinoma (HCC) have not been assessed. Most recently, CDCP1 was identified as a specific target gene of HIF-2α in clear cell renal carcinoma (CC-RCC). However, considering the role of HIF-2α in the progression of HCC is highly controversial, it is necessary to figure out whether HIF-2α and CDCP1 play a significant part in the metastasis of HCC. Our results showed that HIF-2α and CDCP1 were both induced by hypoxia, and the activation of CDCP1 was HIF-2α dependent. CDCP1 was governed by HIF-2α at mRNA and protein levels in HCC cell lines. Moreover, knocking down of HIF-2α not only inhibited cell invasion but also impaired the expression of Tyr(311) phosphorylation of protein kinase Cδ (PKCδ) which is a downstream factor of CDCP1 and has been reported to induce malignant migration in various tumors. Analysis of human HCC samples showed a negative correlation of CDCP1 expression with disease-free survival, and CDCP1 was an independent prognostic factors of disease-free survival. Taken together, these data demonstrated that HIF-2α could promote HCC cell migration by regulating CDCP1, and targeting HIF-2α-CDCP1-PKCδ pathway might be effective to inhibit HCC metastasis. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 20 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 5 | 25% |
| Student > Ph. D. Student | 4 | 20% |
| Student > Master | 4 | 20% |
| Student > Bachelor | 3 | 15% |
| Other | 2 | 10% |
| Other | 1 | 5% |
| Unknown | 1 | 5% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 6 | 30% |
| Medicine and Dentistry | 5 | 25% |
| Agricultural and Biological Sciences | 3 | 15% |
| Immunology and Microbiology | 1 | 5% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 5% |
| Other | 2 | 10% |
| Unknown | 2 | 10% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 27 August 2015.
All research outputs
#20,290,425
of 22,826,360 outputs
Outputs from Tumor Biology
#1,834
of 2,622 outputs
Outputs of similar age
#224,706
of 267,563 outputs
Outputs of similar age from Tumor Biology
#121
of 186 outputs
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