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.2017 Oct 24:16:1165-1176.
doi: 10.17179/excli2017-690. eCollection 2017.

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

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

Yongqing Wei et al. EXCLI J..

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 cancerin 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. Thein vitro 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.

Keywords: SLC39A7; apoptosis; cell proliferation; cervical cancer; invasion; migration.

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Figures

Figure 1
Figure 1. SCL39A7 is upregulated in cervical cancer tissues. The mRNA expression of SCL39A7 was analyzed in Oncomine datasets including (A) Zhai Cervix, (B) Scotto Cervix 2 and (C) Biewenga Cervix.
Figure 2
Figure 2. Silencing of SCL39A7 expression in cervical cancer cells by sh-SCL39A7 transfection. (A) The expression of SCL39A7 mRNA was determined in several cervical cancer cell lines (HeLa, SiHa, CaSki, ME-180) and a normal cervical epithelial cell line H8 by qRT-PCR analysis. (B) Western blot analysis of SCL39A7 protein levels in HeLa and ME-180 cells following sh-SCL39A7#2 infection. The qRT-PCR analysis of SCL39A7 mRNA levels in HeLa (C) and ME-180 (D) following sh-SCL39A7#2 infection; Values were expressed as mean ± standard deviation (SD). ***p < 0.001 compared to negative control (NC)
Figure 3
Figure 3. Silencing of SCL39A7 inhibited cell proliferation in cervical cancer cells. CCK-8 assay was used to determine cell viability in HeLa (A) and ME-180 (B) following sh-SCL39A7#2 infection. Colony formation assay was performed to evaluate cell proliferation ability in HeLa (C) and ME-180 (D) following sh-SCL39A7#2 infection. Values were expressed as mean ± standard deviation (SD). ***p < 0.001 compared to negative control (NC)
Figure 4
Figure 4. Silencing of SCL39A7 induced apoptosis in cervical cancer cells. Cell apoptosis was analyzed by Annexin V/7-AAD staining and flow cytometry in HeLa (A) and ME-180 (B) cells following transfection with lentivirus containing sh-SCL39A7#2 or NC. Values were expressed as mean ± standard deviation (SD). ***p < 0.001 compared to negative control (NC)
Figure 5
Figure 5. Silencing of SCL39A7 suppressed cell migration and invasion in cervical cancer cells. (A) Effect of SCL39A7 knockdown on cell migration of HeLa and ME-180 after sh-SCL39A7#2 transfection. (B) Effect of SCL39A7 knockdown on cell invasion of HeLa and ME-180 after sh-SCL39A7#2 transfection. Values were expressed as mean ± standard deviation (SD). ***p < 0.001 compared to negative control (NC)
Figure 6
Figure 6. Effect of SCL39A7-silencing on its downstream molecular associated with cell apoptosis and migration regulation in HeLa (A) and ME-180 (B), as confirmed by Western blot analysis. GAPDH was used as internal control.
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