Abstract
Research QuestionThe expression of the long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) in embryonic tissues is higher than that in most cancer tissues, such as bladder cancer, indicating that RNA is a carcinoembryonic antigen. However, there are no published reports on the role of UCA1 in endometriosis (EMS). Therefore, to address this gap in knowledge, we assessed the potential role of lncRNA UCA1 in the pathogenesis and progression of EMS.DesignTo verify the expression of UCA1 in EMS, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used. RNA interference (siRNA) was used to study the biological function of UCA1 in EMS in vitro.ResultsqRT-PCR analysis showed that the expression of lncRNA UCA1 in EMS was increased (P<0.01). Knockdown of UCA1 in vitro significantly inhibited the proliferation of endometrial stromal cells (ESCs) and induced autophagy and apoptosis.ConclusionUCA1 is highly expressed in EMS and promotes the proliferation of ESCs but suppresses autophagy and apoptosis. In EMS, UCA1 may be a prognostic marker and therapeutic target.
Highlights
Endometriosis (EMS) is a common benign gynecological disease that is estrogen-dependent
We studied the effect of urothelial carcinoma-associated 1 (UCA1) on the proliferation, autophagy and apoptosis of Endometrial stromal cell (ESC) in vitro
Expression of Long noncoding RNAs (lncRNAs) UCA1 in EMS Tissue qRT-PCR revealed that the expression of lncRNA UCA1 was significantly higher in the eutopic endometrium of patients with endometriosis (0.965 ± 0.105) than in normal endometrial tissues (0.196 ± 0.079) (P
Summary
Endometriosis (EMS) is a common benign gynecological disease that is estrogen-dependent. The growth and proliferation of endometrial tissues or cells outside the uterus, most commonly in the ovaries and pelvic peritoneum, are characteristic of EMS. Under the influence of the disease, 70% of the patients suffer from chronic pelvic pain and 48% have fertility problems [1]. The most generally acknowledged hypothesis about the pathogenesis of EMS is the implantation and growth of disseminated endometrial fragments and viable cells after retrograde flow of menses during menstruation [2]. Menstrual reflux is accepted, it does explain why 90% of women experience menstrual retrograde but that only 10% develop the disease [3].
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