Knockdown of SLC39A7 suppresses cell proliferation, migration and invasion in cervical cancer

Abstract

Cervical cancer is the fourth leading cause of malignancy related mortality in women worldwide. SLC39A7 (ZIP7) is a zinc transporter that plays a key role in intestinal epithelial self-renewal. However, whether or not SLC39A7 is involved in human cervical cancer remains unclear. In this study, we investigated the effects of SLC39A7 in cervical cancer in vitro and elucidate related underlying mechanisms. Using Oncomine data analysis, we first found SLC39A7 is commonly upregulated in cervical cancer tissues in comparison with corresponding normal controls. The in vitro experiments indicated that silencing of SLC39A7 expression resulted in decreased cell pro- liferation, increased cell apoptosis, and attenuated migratory and invasive ability using CCK-8, colony formation, flow cytometry, transwell assays, respectively in cervical cancer cell lines, HeLa and ME-180 cells. In molecular levels, Western blot further demonstrated that silencing of SLC39A7 significantly upregulated the expression of Bax and E-cadherin, downregulated the expression of Bcl-2 and MMP-2 in both HeLa and ME-180 cells. These findings provide evidence that SLC39A7 plays a positive role in the progression of cervical cancer and its knock- down might be as a potential therapeutic target for cervical cancer treatment.