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. 2014 Jan 22;9(1):e86871.
doi: 10.1371/journal.pone.0086871. eCollection 2014.

MiR-26a promotes ovarian cancer proliferation and tumorigenesis

Wenjing Shen  1 , Min Song  2 , Jie Liu  3 , Guangrong Qiu  4 , Tianren Li  1 , Yanjie Hu  1 , Hongbo Liu  5
Affiliations

MiR-26a promotes ovarian cancer proliferation and tumorigenesis

Wenjing Shen et al. PLoS One. .

Abstract

MicroRNAs (miRNAs) important for posttranscriptional gene expression are involved in the initiation and progression of human cancer. In this study, we reported that miR-26a was over-expressed in human EOC specimens and the expression level of extracellular miR-26a in plasma can distinguish patients from healthy controls in EOC. Ectopic expression of miR-26a in ovarian cancer (OC) cells increased cell proliferation and clonal formation. This growth promoting effect of OC cell growth was mediated by miR-26a inhibition of the posttranscription of ER-α. Furthermore, inhibition of miR-26a suppressed the tumor formation generated by injecting OC cells in nude mice. Our results suggest that aberrantly expressed miR-26a may contribute to OC development.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. The expression of miR-26a was increased in EOC patients.
(A)Quantitative analysis of the expression levels of miR-26a in EOC samples normalized to those of 18s rRNA by qRT-PCR. Data for each dot were mean value of one sample repeated in three independent experiments (normal, n = 19; tumor, n = 26). **P<0.01 vs Normal. (B)Quantitative analysis of the expression levels of plasma miR-26a by qRT-PCR. Data for each dot were mean value of one sample repeated in three independent experiments (normal, n = 13; tumor, n = 17).
Figure 2
Figure 2. MiR-26a promoted EOC cell growth.
Growth curves of SKOV3 (A) or ES2 (B) cells transfected with miR-26a (left panel) or anti-miR-26a (right panel). Cell numbers were normalized to those in 0 hr. Data were mean±s.e. of three independent experiments in triplicate. *p<0.05, **p<0.01 vs empty vector (Ctrl) or negative control (NC). (C) Cell proliferation transfected with miR-26a was measured by a WST-1 assay. Data were mean±s.e. of three independent experiments in triplicate. **p<0.01 vs empty vector (Ctrl) (D) Quantification of the colonies formed by Ctrl or miR-26a transfected cells. Data were mean±s.e. of three independent experiments. **P<0.01 vs Ctrl.
Figure 3
Figure 3. ERα was a target of miR-26a.
(A) Stable 1 cells (S1) were transfected with pGL3-ERα-WT (WT) reporter vector or pGL3-ERα-Mut (MUT). Data were mean±s.e. of three independent experiments. **P<0.01 vs control cells (Ctrl). (B) Quantitative analysis of the expression levels of ERα in Stable1 (S1), Stable2 (S2) and control (Ctrl) cells were determined and normalized to GAPDH mRNA levels. *p<0.05,**P<0.01 vs Ctrl. (C) Western-blot analysis of total cell lysates extracted from indicated stable cells using the indicated antibodies. Data was representative of three independent experiments and quantitation normalized with the Ctrl. Tubulin served as a loading control. (D) The growth curves of S1, S2 and Ctrl cells. Data were mean±s.e. of three independent experiments in triplicate. *p<0.05, **P<0.01 vs Ctrl. (E) Over-expression of ERα decreased the growth of S1 cells after transfection. Cell numbers were normalized to Ctrl cells. Data were mean±s.e. of three independent experiments in triplicate.
Figure 4
Figure 4. MiR-26a promoted the development of tumor in nude mice.
Tumor formation generated by the SKOV3 cells. (A) transfected with miR-26a or anti-miR-26a(B) Nude mice were subcutaneously injected with 2×106 transfected cells. Representative images, measurement of the final volume and weight of the tumors formed. The tumor sizes were measured and calculated in Materials and methods. Data were mean±s.d. of 4–6 mice. **P<0.01 vs empty vector or nonsense.
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Grants and funding

This work was sponsored by grants from the Project No. 30571836 from the NNSF(National Natural Science Foundation) of China. In addition, the work presented is part of projects with Project No.L2010681 financially supported by Science Foundation of the Education Department of Liaoning Province of China, and Project No.201202259 financially supported by Science Foundation of Science and Technology Bureau of Liaoning Province of China. Author Min Song contributed to experimental conceiving and design, guidance and discussion of the project, so she is the co-correspondence author of this paper. All the other funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.