Wei Yongqing, Dong Jie, Li Fuli, Wei Zhuqing, Tian Yuling
Department of Gynecology and Obstetrics, Jinan Central Hospital Affiliated to Shandong University, Jinan 250012, China.
Department of Stomatology, Chengyang People's Hospital, Qingdao 266109, China.
EXCLI J. 2017 Oct 24;16:1165-1176. doi: 10.17179/excli2017-690. eCollection 2017.
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 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 experiments indicated that silencing of SLC39A7 expression resulted in decreased cell proliferation, 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 knockdown might be as a potential therapeutic target for cervical cancer treatment.
宫颈癌是全球女性恶性肿瘤相关死亡的第四大主要原因。溶质载体家族39成员7（SLC39A7，即ZIP7）是一种锌转运蛋白，在肠道上皮自我更新中起关键作用。然而，SLC39A7是否参与人类宫颈癌尚不清楚。在本研究中，我们调查了SLC39A7在宫颈癌中的作用，并阐明相关潜在机制。通过Oncomine数据分析，我们首先发现与相应正常对照相比，SLC39A7在宫颈癌组织中普遍上调。实验表明，在宫颈癌细胞系HeLa和ME-180细胞中，分别使用CCK-8、集落形成、流式细胞术、Transwell实验，沉默SLC39A7表达导致细胞增殖减少、细胞凋亡增加以及迁移和侵袭能力减弱。在分子水平上，蛋白质印迹进一步证明，在HeLa和ME-180细胞中，沉默SLC39A7显著上调Bax和E-钙黏蛋白的表达，下调Bcl-2和MMP-2的表达。这些发现提供了证据，表明SLC39A7在宫颈癌进展中起积极作用，其敲低可能作为宫颈癌治疗的潜在靶点。
