Abstract | AIMS: METHODS AND RESULTS: We confirmed that AGXT2L1 was down-regulated in liver cancer samples by immunohistochemical (IHC) staining. We also demonstrated that this down-regulation was associated with several clinicopathological features such as alpha fetoprotein (AFP) serum level and T stage. Furthermore, we showed with Kaplan-Meier analysis that expression of AGXT2L1 in tumour samples was significantly correlated with patient prognosis. The bioinformatic tool indicated that AGXT2L1 plays a role in the lipid metabolic process of HCC tissue, while siRNA silenced the expression of AGXT2L1 in HCC 97H and LM3 cells, confirming that down-regulation of AGXT2L1 promotes the lipogenesis of cancer cells. CONCLUSIONS: For the first time, we have shown that AGXT2L1 is down-regulated in HCC and its low expression indicates a poor prognosis. Our findings also demonstrated that AGXT2L1 is a crucial gene in the abnormal lipogenesis of HCC tissue.
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Authors | Qianshan Ding, Jian Kang, Jinfen Dai, Meng Tang, Qi Wang, Haotian Zhang, Wenyi Guo, Rongze Sun, Honggang Yu |
Journal | Journal of clinical pathology
(J Clin Pathol)
Vol. 69
Issue 3
Pg. 215-20
(Mar 2016)
ISSN: 1472-4146 [Electronic] England |
PMID | 26294768
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ |
Chemical References |
- AFP protein, human
- alpha-Fetoproteins
- Transaminases
- Alanine-glyoxylate transaminase
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Topics |
- Carcinoma, Hepatocellular
(enzymology, genetics, mortality, pathology, therapy)
- Cell Line, Tumor
- Computational Biology
- Databases, Genetic
- Down-Regulation
- Female
- Gene Expression Regulation, Enzymologic
- Gene Expression Regulation, Neoplastic
- Humans
- Kaplan-Meier Estimate
- Lipogenesis
- Liver Neoplasms
(enzymology, genetics, mortality, pathology, therapy)
- Male
- Middle Aged
- Neoplasm Staging
- RNA Interference
- Signal Transduction
- Time Factors
- Transaminases
(genetics, metabolism)
- Transfection
- Treatment Outcome
- alpha-Fetoproteins
(analysis)
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