Abstract
MicroRNAs play key roles in tumor proliferation and invasion. Here we show distinct expression of miR-222-3p between ERα-positive and ERα-negative endometrial carcinoma (EC) cell lines and primary tumors, and investigation of its relationship with ERα and other clinical parameters. In vitro, the function of miR-222-3p was examined in RL95-2 and AN3CA cell lines. MiR-222-3p expression was negatively correlated with ERα. Over-expressed miR-222-3p in RL95-2 cells promoted cell proliferation, enhanced invasiveness and induced a G1 to S phase shift in cell cycle. Furthermore, the miR-222-3p inhibitor decreased the activity of AN3CA cells to proliferate and invade. In vivo, down-regulated miR-222-3p of AN3CA cells inhibited EC tumor growth in a mouse xenograft model. Additionally, miR-222-3p increased raloxifene resistance through suppressing ERα expression in EC cells. In conclusion, miR-222-3p plays a significant role in the regulation of ERα expression and could be potential targets for restoring ERα expression and responding to antiestrogen therapy in a subset of ECs.
Highlights
endometrial carcinoma (EC) is the most common malignancy of the female genital system, with estimated 8,190 deaths in the USA in 2013 [1]
Expression of miR-222-3p is up-regulated in EC Our results showed that miR-222-3p expression was much lower in estrogen receptor alpha (ERa)-positive than in ERa-negative EC tissue samples (P,0.0001, Fig. 1A), and level of miR-222-3p expression was correlated inversely with ERa expression (Fig. 1A)
Since miR222-3p was higher in ERa negative ECs than in ERa positive cases, we further studied miR-222-3p expression level and its association with clinicopathologic parameters in ECs
Summary
EC is the most common malignancy of the female genital system, with estimated 8,190 deaths in the USA in 2013 [1]. Further elucidation of the molecular mechanisms during endometrial cancer is urgently required
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