Abstract
ST3Gal IV is one of the principal sialyltransferases responsible for the biosynthesis of α2, 3-sialic acid to the termini N-glycans or O-glycans of glycoproteins and glycolipids. It has been reported that ST3Gal IV expression is associated with gastric carcinoma, pancreatic adenocarcinoma and breast cancer. While the expression and functions of ST3Gal IV in cervical cancer are still poorly understood. In this study, we found that ST3Gal IV was downregulated in human cervical cancer tissues compared to normal cervix tissues, and ST3Gal IV expression was negatively associated with the pathological grade of cervical cancer. ST3Gal IV upregulation inhibited the growth and proliferation of cervical cancer HeLa and SiHa cells in vitro and in vivo. Furthermore, ST3Gal IV overexpression enhanced the expression of several Notch pathway components such as Jagged1, Notch1, Hes1 and Hey1, while cell cycle protein expression like Cyclin D1, Cyclin E1, CDK2 and CDK4 were decreased. These results indicate that expression of ST3Gal IV is reduced in cervical cancer and plays a negative role in cell proliferation via Notch/p21/CDKs signaling pathway. Thus, sialyltransferase ST3Gal IV might be a target for the diagnosis and therapy of cervical cancer.
Highlights
Cervical cancer is one of the leading causes of cancer death among females, and its death rate ranks second among cancers in less developed countries [1]
The association between ST3Gal IV expression and patient ages, pathological types, pathological grading, primary tumor stages and lymph node metastasis was assessed by Pearson’s chi-squared test (Figure 1C). These results suggest that ST3Gal IV expression was negatively correlated with pathological grading of cervical cancer tissues (p = 0.005)
We detected the expression level of ST3Gal IV in cervical cancer tissue microarray (n = 75), finding low ST3Gal IV expression in the cervical cancer tissues compared to normal cervix tissues
Summary
Cervical cancer is one of the leading causes of cancer death among females, and its death rate ranks second among cancers in less developed countries [1]. It has been demonstrated that cervical cancer is caused by human papillomavirus (HPV) infection [2]. Significant advances have been made in cervical cancer screening and treatment. The development of HPV and its widespread adoption may contribute to reduced incidence of the disease. The incidence and mortality rates are still high due to the difficulties in achieving widespread compliance with HPV vaccination [3]. HPV vaccines cannot protect against all the types of HPV that cause cervical cancer [1]
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