Abstract
Our previous study showed DNMT1 is up-regulated in esophageal squamous cell carcinoma (ESCC), which is associated with methylation of tumor suppressors. In the current study, we investigate the role of DNMT1 in ESCC. We found silencing DNMT1 inhibited proliferation, metastasis and invasion of three different ESCC cells, K150, K410 and K450. We also found silencing DNMT1 induced G1 arrest and cell apoptosis in K150, K410 and K450 cells. In vivo study showed silencing DNMT1 suppressed tumor growth in nude mice. In addition, silencing DNMT1 increased expression of tumor suppressor genes, RASSF1A and DAPK, in ESCC cells and ESCC xenograft in nude mice. Moreover, silencing DNMT1 decreased methylation in promoter of RASSF1A and DAPK. In conclusion, our data demonstrated that silencing DNMT1 inhibits proliferation, metastasis and invasion in ESCC by suppressing methylation of RASSF1A and DAPK.
Highlights
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies in worldwide
Our previous study showed DNA methyltransferase 1 (DNMT1) is up-regulated in esophageal squamous cell carcinoma (ESCC), which is associated with methylation of tumor suppressors
In order to investigate the role of DNMT1 in ESCC, we examined the effects of silencing DNMT1 on proliferation, metastasis and invasion in ESCC cells
Summary
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies in worldwide. The incidence of ESCC in China is much higher than other countries. Numerous efforts had been made, the mechanism of ESCC is not fully understood yet. Promoter methylation of tumor suppressor genes is a critical early step in carcinogenesis including that of ESCC. Our previous study indicates that the status of promoter methylation changes following the progression of ESCC. P16 methylation is a frequent and early event in ESCC. Methylation of MLH1 was associated with advanced stage ESCC. The aberrant methylation of tumor suppressor genes has been used as a predictor of the clinical outcome following a curative resection of ESCC. Promoter methylation of APC and FHIT has been associated with reduced survival in ESCC patients after esophagectomy
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