Background and purpose: 5-Azacytidine(5-azaC) is a DNA methyltransferase inhibitor

and has been used to treat many kinds of malignant tumors. However

studies on the role of 5-azaC in esophageal cancer are insufficient. Evading apoptosis is a major feature of tumors and also a hot spot for anti-tumor therapy. Notch1 signaling pathway is one of the most important pathways involved in initiation and development of esophageal cancer

and is closely related to cell proliferation

invasion and apoptosis. This study aimed to investigate the influence of 5-azaC on cell apoptosis and Notch1 signaling pathway in esophageal cell lines

so as to explore the possible mechanism of treatment with 5-azaC. Methods: TE-1 and OE33 cell lines were treated with 5-azaC in a concentration of 50 μmol/L and inhibitory effects of 5-azaC in esophageal cell lines were estimated using cell counting kit-8 (CCK-8). Then cell morphology was visualized using optical microscopy. Flow cytometry and Western blot were used to determine apoptotic rate and to analyze expression of B-cell lymphoma-extra large (BCL-XL)

an anti-apoptosis protein

respectively. And finally

realtime fluorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot were employed to explore expression changes of Notch1 and Notch intracellular domain (NICD). Results: 5-AzaC was able to induce apoptosis

and had a remarkable inhibitory effect on esophageal squamous carcinoma TE-1 and adenocarcinoma cell line OE33. Increased mRNA expression of Notch1 was observed following treatment with 5-azaC

while protein expression of Notch1 was unchanged and NICD showed significant decline in TE-1 and OE33 cell lines. Conclusion: 5-AzaC has strong apoptosis-promoting effect on both esophageal squamous carcinoma TE-1 and adenocarcinoma cell line OE33

and the mechanism may be related to the inhibition of Notch1 signaling pathway via downregulating NICD protein.