期刊
ONCOTARGET
卷 7, 期 10, 页码 11194-11207出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.7156
关键词
pancreatic cancer; enhancer of zeste homolog 2; metastasis associated lung adenocarcinoma transcript 1; long non-coding RNA; cell migration
资金
- National Natural Science Foundation of China [81502017, 81502018, 81572315, 81171887, 91229117]
- Program of Shanghai Subject Chief Scientist [12XD1404200]
- Shanghai International Science and Technology Cooperation Project [12410709000]
- Shanghai Science and Technology Committee [11DZ1922002]
- Shanghai Hospital Development Center [SHDC12014128]
- National Key Clinical Discipline-Oncology
- Songjiang Liandong Program [0702N14002]
Enhancer of zeste homolog 2 (EZH2) is an essential component of the polycomb repressive complex 2 (PRC2), which is required for epigenetic silencing of target genes, including those affecting cancer progression. Its role in pancreatic cancer remains to be clarified; therefore, we investigated the effects of aberrantly expressed EZH2 on pancreatic cancer. We found that EZH2 expression is up-regulated in pancreatic cancer tissues and positively correlated with lymph node metastasis and advanced clinical stage in pancreatic cancer patients. EZH2 knockdown in pancreatic cancer cell lines inhibited cell migration and invasion, but did not alter cell proliferation. Silencing of EZH2 also increased E-cadherin expression in vitro, and E-cadherin expression was inversely correlated with EZH2 expression in pancreatic cancer tissue samples. Patients with high EZH2 and low E-cadherin expression had the worst prognosis. RIP and ChIP assays suggest that EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression. Our results show that EZH2-based therapies may be an option for the treatment of pancreatic cancer.
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