| Title |
18F-Fluorodeoxyglucose uptake on positron emission tomography/computed tomography is associated with metastasis and epithelial-mesenchymal transition in hepatocellular carcinoma
|
|---|---|
| Published in |
Clinical & Experimental Metastasis, April 2017
|
| DOI | 10.1007/s10585-017-9847-9 |
| Pubmed ID | |
| Authors |
Misu Lee, Jeong Yong Jeon, Micheal L. Neugent, Jung-Whan Kim, Mijin Yun |
| Abstract |
Hepatocellular carcinoma (HCC) is the fifth leading cause of cancer mortality worldwide. Several studies have investigated the relationship between (18)F-fluorodeoxyglucose ((18)F-FDG) uptake on positron emission tomography and the prognosis of patients with HCC, although the relationship between (18)F-FDG uptake and expression of EMT-related proteins in these patients remains unclear. We retrospectively enrolled 116 patients with HCC treated by curative surgical resection and who underwent (18)F-FDG positron emission tomography/computed tomography (PET/CT) for preoperative staging. The relationship between the tumor-to-liver standardized uptake value ratio (TLR) and the presence of metastasis was determined. By using HCC cell lines with different (18)F-FDG uptake, we assessed the effect of (18)F-FDG uptake on in vitro cell proliferation and migration on the inhibition of glucose uptake. Ten (29.4%) of 34 patients with high TLRs had extrahepatic metastases, whereas six (7.3%) of 82 patients with low TLRs had extrahepatic metastases (p = 0.002). Hepatocellular carcinomas with high TLRs showed higher expression of glucose transporter isoform 1 and EMT markers than did HCCs with low TLRs. After treatment with a glucose uptake inhibitor, HCC cells with high (18)F-FDG uptake showed decreased cell proliferation and migration and a reversal in the expression of EMT markers. High (18)F-FDG uptake on PET/CT is associated with frequent extrahepatic metastasis and EMT in patients with HCC. Inhibition of glucose uptake reduced cell proliferation, reversed EMT-related protein expression, and decreased cellular migration. Glycolytic regulation could be a new therapeutic target to reduce tumor growth and metastatic potential in HCCs with a high glycolytic phenotype. |
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 9 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Other | 2 | 22% |
| Researcher | 2 | 22% |
| Student > Bachelor | 1 | 11% |
| Student > Doctoral Student | 1 | 11% |
| Student > Master | 1 | 11% |
| Other | 1 | 11% |
| Unknown | 1 | 11% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 5 | 56% |
| Psychology | 1 | 11% |
| Biochemistry, Genetics and Molecular Biology | 1 | 11% |
| Unknown | 2 | 22% |
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 22 April 2017.
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#19,382,126
of 23,854,458 outputs
Outputs from Clinical & Experimental Metastasis
#603
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#239,711
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Outputs of similar age from Clinical & Experimental Metastasis
#4
of 6 outputs
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