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Original Article
- SIRT7, H3K18ac, and ELK4 Immunohistochemical Expression in Hepatocellular Carcinoma
- Hye Seung Lee, Wonkyung Jung, Eunjung Lee, Hyeyoon Chang, Jin Hyuk Choi, Han Gyeom Kim, Aeree Kim, Baek-hui Kim
- J Pathol Transl Med. 2016;50(5):337-344. Published online August 5, 2016
- DOI: https://doi.org/10.4132/jptm.2016.05.20
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- 23 Web of Science
- 25 Crossref
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Abstract
PDF - Background
SIRT7 is one of the histone deacetylases and is NAD-dependent. It forms a complex with ETS-like transcription factor 4 (ELK4), which deacetylates H3K18ac and works as a transcriptional suppressor. Overexpression of SIRT7 and deacetylation of H3K18ac have been shown to be associated with aggressive clinical behavior in some cancers, including hepatocellular carcinoma (HCC). The present study investigated the immunohistochemical expression of SIRT7, H3K18ac, and ELK4 in hepatocellular carcinoma.
Methods
A total of 278 HCC patients were enrolled in this study. Tissue microarray blocks were made from existing paraffin-embedded blocks. Immunohistochemical expressions of SIRT7, H3K18ac and ELK4 were scored and analyzed.
Results
High SIRT7 (p = .034), high H3K18ac (p = .001), and low ELK4 (p = .021) groups were associated with poor outcomes. Age < 65 years (p = .028), tumor size ≥ 5 cm (p = .001), presence of vascular emboli (p = .003), involvement of surgical margin (p = .001), and high American Joint Committee on Cancer stage (III&V) (p < .001) were correlated with worse prognoses. In multivariate analysis, H3K18ac (p = .001) and ELK4 (p = .015) were the significant independent prognostic factors.
Conclusions
High SIRT7 expression with poor overall survival implies that deacetylation of H3K18ac contributes to progression of HCC. High H3K18ac expression with poor prognosis is predicted due to a compensation mechanism. In addition, high ELK4 expression with good prognosis suggests another role of ELK4 as a tumor suppressor beyond SIRT7’s helper. In conclusion, we could assume that the H3K18ac deacetylation pathway is influenced by many other factors. -
Citations
Citations to this article as recorded by
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Case Report
- Mineralizing Pulmonary Elastosis Associated with a Giant Cell Carcinoma.
- Min Kyung Kim, Kwang Il Kim, Min Joo Kim, Young Woo Suh, Il Hun Seo, Hyun Ju Lee, Han Gyeom Kim
- Korean J Pathol. 1998;32(9):691-693.
- 1,702 View
- 10 Download
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Abstract
- Mineralizing pulmonary elastosis is a result of chronic alveolar hemorrhage forming iron encrustation of a pulmonary elastic tissue. It has been reported as a complication of some diseases such as bronchiectasis, idiopathic pulmonary hemosiderosis, and cardiac failure. It is extremely rare to occur with a giant cell carcinoma as we experienced. A 59 year-old man visited our hospital for cough and blood tinged sputum. A chest CT scan revealed 10 9 6 cm sized round mass in the left upper lobe. He had lobectomy of left upper lobe, but died of respiratory failure at the postoperative eighteenth day. The lung showed a necrotic tumor and a yellow tan consolidation around the mass. Microscopically, the tumor was composed of nests or syncytia of large bizarre cells and tumor giant cells, and was diagnosed as a giant cell carcinoma. Interestingly, in the surrounding lung parenchyma there were a lot of foreign body type giant cells phagocytizing iron encrustated elastic fibers, which were easily identified by elastic van Gieson and prussian blue stains. Those degenerated elastic fibers appeared in pulmonary interstitial tissue as well as blood vessel walls. The authors concluded tumoral hemorrhage and necrosis resulted in mineralizing pulmonary elastosis.
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