High expression of lysine-specific demethylase 1 correlates with poor prognosis of patients with esophageal squamous cell carcinoma
•Upregulation of LSD1 correlates with lymph node metastasis in ESCC.•LSD1 overexpression predicts poor prognosis in ESCC patients.•LSD1 knockdown using LSD1-specific shRNAs inhibited motility and invasion in ESCC.•A LSD1 inhibitor tranylcypromine attenuated migration and invasiveness. Recent studies...
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Published in | Biochemical and biophysical research communications Vol. 437; no. 2; pp. 192 - 198 |
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Main Authors | , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
26.07.2013
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Subjects | |
Online Access | Get full text |
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Summary: | •Upregulation of LSD1 correlates with lymph node metastasis in ESCC.•LSD1 overexpression predicts poor prognosis in ESCC patients.•LSD1 knockdown using LSD1-specific shRNAs inhibited motility and invasion in ESCC.•A LSD1 inhibitor tranylcypromine attenuated migration and invasiveness.
Recent studies have elucidated the role of lysine-specific demethylase 1 (LSD1), a member of the histone demethylases, in epigenetic regulation of tumor suppressing/promoting genes and neoplastic growth. However, the expression of LSD1 in patients with esophageal squamous cell carcinoma (ESCC) is still unknown. Here, we reported that LSD1 expression was elevated in cancerous tissue and correlated with lymph node metastasis and poorer overall survival in patients with ESCC. Compared to EC109 cells, LSD1 expression was unregulated in aggressive cancer cell lines KYSE450 and KYSE150. Knockdown of LSD1 using lentivirus delivery of LSD1-specific shRNA abrogated the migration and invasion of ESCC cells in vitro. Further, a LSD1 inhibitor, tranylcypromine, suppressed H3K4me2 demethylation and attenuated cellular motility and invasiveness in a dose-dependent manner. Taken together, these data suggested that LSD1 was a potential prognostic maker and may be a molecular target for inhibiting invasion and metastasis in ESCC. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2013.05.123 |