Abstract
The molecular mechanisms by which uterine leiomyoma (UL) cells proliferate are unclear. Long noncoding RNA (lncRNA) is reported to participate in the occurrence and development of gynecological cancers. We investigated the molecular mechanisms that lncRNA uses in UL. We found that lncRNA Alu-mediated p21 transcriptional regulator (APTR) showed higher expression in UL tumor tissues compared with that in normal uterine tissues. APTR induced cell proliferation and colony formation both in vitro and in vivo. The JASPAR database showed that APTR was likely interacted with ERα, and these molecules were identified via laser scanning confocal microscopy and RNA immunoprecipitation analysis. To verify the correlation between APTR and ERα, we overexpressed and underexpressed APTR and simultaneously expressed ERα. The results showed that APTR function was suppressed. APTR increased the expressions of the proteins in the Wnt pathway, and inhibiting ERα eliminated these responses. In conclusion, our data suggest that APTR promoted leiomyoma cell proliferation through the Wnt pathway by targeting ERα, suggesting a new role of APTR in the Wnt signaling pathway in UL.
Highlights
Uterine leiomyoma (UL) is the most common benign gynecological tumor, with an incidence rate of 30–40% in fertile women [1]
We identified a new effect of Long noncoding RNA (lncRNA) Alu-mediated p21 transcriptional regulator (APTR), which targets the p21 promoter
Knocking down the ERa level abolished the effect of APTR on UL cell proliferation
Summary
Uterine leiomyoma (UL) is the most common benign gynecological tumor, with an incidence rate of 30–40% in fertile women [1]. UL may lead to asymptomatic complications such as uterine bleeding, severe dysmenorrhea, pelvic pain and infertility and is the leading indication for a hysterectomy [2]. Because the typical marriage age has increased, and many women have not completed childbearing, hysterectomies are often contraindicated [3]. In vitro and in vivo experiments have shown that UL is an estrogen-dependent tumor, and estrogen affects UL promotion and progression [4]. Estrogen binds to its receptors and initiates transcription, promotes UL cell proliferation [5]. Whether ERa or ERb mediate estrogen function and how estrogen affects UL cell proliferation remain unclear
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