The influence of SnoN gene silencing by siRNA on the cell proliferation and apoptosis of human pancreatic cancer cells
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RESEARCH
Open Access
The influence of SnoN gene silencing by siRNA on the cell proliferation and apoptosis of human pancreatic cancer cells Chengli Liu1*, Hui Zhang1, Xiaoxia Zang2, Cheng Wang1, Yalin Kong1 and Hongyi Zhang1
Abstract Background: The prognosis for pancreatic cancer (PC) is very poor. The SnoN gene may have a role in cell proliferation and apoptosis in human cancer. However, the influence of SnoN on cell proliferation and apoptosis in human PC cells remains unknown. Methods: SnoN expression was assessed in SW1990 PC cell lines using real-time polymerase chain reaction (PCR). A luciferase reporter assay was used to confirm the target associations. The effect of SnoN on cell proliferation in vitro was confirmed using Cell Counting Kit-8. Apoptosis was confirmed using flow cytometry. Gene and protein expression were examined using real time PCR and Western blotting, respectively. Results: SnoN siRNA significantly inhibited the growth of SW1990 cells by decreasing cell proliferation (P < 0.05) and increasing cell apoptosis (P < 0.05), compared with the blank group and the negative control group. The highest inhibition of cell proliferation appeared at 3 days post-transfection. Cell apoptosis more obvious at 48 h after transfection. Conclusions: In summary, our results reveal that the RNAi-mediated downregulation of SnoN effectively inhibited the proliferation of PC cells. SnoN-siRNA also enhanced SW1990 PC cell apoptosis. These findings indicate that SnoN gene plays an important role in pancreatic cancer development, and might serve as a potential therapeutic target for pancreatic cancer. However, further in vivo studies are needed to clarify the influence of SnoN gene silencing by siRNA on pancreatic cancer therapy. Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx. eu/vs/7609324661510147 Keywords: SnoN gene, Proliferation, Apoptosis, Pancreatic cancer (PC)
Background Pancreatic cancer (PC) is one of the most fatal malignant diseases worldwide. The incidence of PC is lower than that of many other types of cancer. However, it is the fourth most common cause of death from cancer [1]. Because of nonspecific incipient symptoms and early metastasis, PC is highly malignant and invasive, resulting in poor prognosis [2]. Previous statistics for 2002–2008 from the US National Cancer Institute showed an overall 5-year relative survival rate of 5.8% and a one-year * Correspondence: [email protected] 1 Department of Hepatobiliary Surgery, Air Force General Hospital of PLA, 30 Fucheng Road, Beijing 100142, China Full list of author information is available at the end of the article
mortality rate of 90%, with a median survival of less than 6 months [3,4]. A number of studies [5-8] have showed that the development and progression of PC are linked with complex gene regulation, such as the inactivation of tumour suppressor genes, the activation of proto-oncogenes, abnormal regulation of cell proliferation and apoptosis adjustment disorders, and abnorma
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