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. 2017 Jul;6(7):1686-1697.
doi: 10.1002/cam4.1110. Epub 2017 Jun 19.

MiR-375/SLC7A11 axis regulates oral squamous cell carcinoma proliferation and invasion (V体育2025版)

Yadong Wu  1   2 , Xiangjie Sun  3   4 , Bin Song  2 , Xiaoling Qiu  1 , Jianjiang Zhao  1
Affiliations

MiR-375/SLC7A11 axis regulates oral squamous cell carcinoma proliferation and invasion

Yadong Wu et al. Cancer Med. 2017 Jul.

Abstract

We aimed to detect the functions of miR-375/SLC7A11 axis on oral squamous cell carcinoma (OSCC) cell proliferation and invasion. Expression levels of miR-375 and SLC7A11 in OSCC tissues and cells were measured with RT-qPCR and western blot. Targeting site was predicted by TargetScan and confirmed by dual luciferase reporting assay. By way of manipulating the expression level of miR-375 and SLC7A11 in CAL-27 and Tca8113 cell lines, the cell biological abilities were evaluated. MTT, colony formation, Transwell, wound healing assays and flow cytometry were used to detect OSCC cell viability, proliferation, invasion, migration and apoptosis, respectively. MiR-375 was significantly downregulated in OSCC tissues and cells compared to adjacent tissue and normal oral cell line respectively while SLC7A11 was upregulated VSports手机版. Targeting relationship was verified by luciferase reporting assay, and miR-375 could effectively suppress SLC7A11 level in OSCC cells. Replenishing of miR-375 significantly repressed OSCC cell viability, proliferation, invasion and migration and induced cell apoptosis and G1/G0 arrest. Overexpression of SLC7A11 recovered those biological abilities in miR-375 upregulated cells. Collective data suggested that miR-375 served as a tumor suppressor via regulating SLC7A11. Replenishing of miR-375 or knockout of SLC7A11 could be therapeutically exploited. .

Keywords: OSCC; SLC7A11; miR-375 V体育安卓版. .

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Figures

Figure 1
Figure 1
MiR‐375 was downregulated in human oral squamous cell carcinoma (OSCC) tissues and cells while SLC7A11 was upregulated. (A) The relative expression level of miR‐375 in 40 paired OSCC tissues and adjacent normal tissues, ** P < 0.05 versus adjacent normal tissues. (B) The relative expression of SLC7A11 mRNA in 40 paired OSCC tissues and adjacent normal tissues, ** P < 0.05 versus adjacent normal tissues. (C) The expression of SLC7A11 protein in OSCC tissues and adjacent normal tissues. (D) The relative expression level of miR‐375 in human OSCC cell lines and normal oral cell line (Hs 680.Tg), ** P < 0.05 versus Hs 680.Tg. (D) The relative expression of SLC7A11 mRNA in normal oral cell line and human OSCC cell lines, ** P < 0.05 versus Hs 680.Tg. (E) The expression of SLC7A11 protein in human OSCC cell lines and normal oral cell line, GAPHD acted as an internal control.
Figure 2
Figure 2
MiR‐375 directly targeted SLC7A11. (A) 3'UTR region of SLC7A11 mRNA is partially complementary to miR‐375. (B) The luciferase activities of HEK293T cells in different groups. (C) The expression of miR‐375 in transfected cells was measured by RT‐qPCR. (D–E) The mRNA expression and protein level of SLC7A11 was evaluated by RT‐qPCR and western blot respectively. ** P < 0.05. All data was presented as Mean ± SD from three independent experiments.
Figure 3
Figure 3
The effects of miR‐375/SLC7A11 axis on oral squamous cell carcinoma (OSCC) cell viability and proliferation. (A) MTT assay was performed to assess cell viability. MiR‐375 and SLC7A11 siRNA significantly lightened OD value of CAL‐27 and Tca8113 cells while pCDNA3.1 accelerated. (B) The effects of miR‐375 and SLC7A11on OSCC cell growth were further confirmed by colony formation. ** P < 0.05 versus NC1 group. All data was presented as Mean ± SD from three independent experiments.
Figure 4
Figure 4
The effects of miR‐375/SLC7A11 axis on oral squamous cell carcinoma cell invasion and migration. (A) At 48 h after transfection, wound healing assay was performed to assess the migration ability of CAL‐27 and Tca8113 cells. (B) At 48 h after transfection, Transwell assay was utilized and the influence of miR‐375/SLC7A11 axis on cell invasive abilities was investigated. ** P < 0.05 versus NC1 group. All data was presented as Mean ± SD from three independent experiments. (C) Wound healing area of all groups was calculated with the help of Adobe Photoshop CS6. (D) After staining the invading cells, cell number of five random fields was calculated and compared. ** P < 0.05 vs. NC1 group. All data was presented as Mean ± SD from three independent experiments.
Figure 5
Figure 5
The effects of miR‐375/SLC7A11 axis on oral squamous cell carcinoma cell mitosis and apoptosis. (A) At 48 h after transfection, PI staining was performed and flow cytometry was utilized to count cells in each phase. G1/G0 arrest was confirmed in cells transfected with miR‐375 mimics and SLC7A11 siRNA. (B) At 48 h after transfection, cells were stained with PI and Annexin V‐FITC and separated by flow cytometry. Cell apoptosis was induced in mimics group and si‐SLC7A11 group. ** P < 0.05 versus NC1 group. All data was presented as Mean ± SD from three independent experiments. (C‐D) Cell cycle and apoptosis was analyzed with FlowJo_V10 and collective data was compared. **P < 0.05 vs. NC1 group. All data was presented as Mean ± SD from three independent experiments.
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