Background: In recent decades, long non-coding RNAs (lncRNAs) have been reported as crucial functional regulators involved in ovarian cancer. In the present study, we explored how lncRNA RHPN1-AS1 influences the progression of epithelial ovarian cancer (EOC) through tumor cell-dependent mechanisms. Results: The expression of RHPN1-AS1 in EOC tissues was higher than that in para-cancerous control tissues. High expression of RHPN1-AS1 was closely associated with poor prognosis in EOC patients. N6methyladenosine (m6A) improved the stability of RHPN1-AS1 methylation transcript by reducing RNA degradation, which resulted in upregulation of RHPN1-AS1 in EOC. In vitro and in vivo functional experiments showed that RHPN1-AS1 promoted EOC cell proliferation and metastasis. RHPN1-AS1 acted as a ceRNA to sponge miR-596, consequently increasing LETM1 expression and activating the FAK/PI3K/Akt signaling pathway. Conclusion: RHPN1-AS1-miR-596-LETM1 axis plays a crucial role in EOC progression. Our findings may provide promising drug targets for EOC treatment. Methods: We determined the aberrantly expressed lncRNAs in EOC via microarray analysis and validated RHPN1-AS1 expression by qRT-PCR. The RHPN1-AS1-miR-596-LETM1 axis was examined by dual-luciferase reporter assay and RIP assay. The mechanism of RHPN1-AS1 was investigated through gain-and loss-offunction studies both in vivo and in vitro.www.aging-us.com 4559 AGING EOC patients, the 5-year OS remains very low [2]. High throughput sequencing technologies made it possible for large-scale access to gene expression profiles. Gene expression microarray provided new insights for the identification of tumor-associated genes, biomarkers, and therapeutic targets [3]. The integration of those databases containing multiple gene expression data of various cancer types allows in-depth analysis of molecular mechanisms.Long non-coding RNAs (lncRNAs) have been widely engaged in various cellular processes, including post-transcriptional regulation via epigenetic regulation [4,5]. In addition, growing evidence has shown that lncRNAs function critically in multiple diseases, especially in cancer occurrence and progression [6,7]. Recently, lncRNAs, such as FLVCR1-AS1, ABHD11-AS1, and NORAD have been found to be associated with tumorigenesis, metastasis, and progression of EOC and are regarded as potential therapeutic targets for EOC [8][9][10]. It has been reported that dysregulation of lncRNAs played essential roles in the development of tumors, including EOC [11]. LncRNA RHPN1-AS1 is an important regulator in cancer development and progression. It has been reported that RHPN1-AS1 enhances cell proliferation, migration, and in cervical cancer via miR-299-3p/FGF2 cascade [12]. RHPN1-AS1 regulates breast cancer cell proliferation via miR-4261/c-Myc axis and modulation of p53 [13]. RHPN1-AS1 also functions in glioma, neck squamous cell carcinoma, gastric cancer, hepatocellular carcinoma, non-small cell lung cancer, and Uveal Melanoma [14][15][16][17][18][19]. However, the function of RHPN1-AS1...

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BackgroundThe long noncoding RNA X-inactive specific transcript (XIST) was reported to play vital roles in tumor progression. In the present study, we determined the regulatory function of XIST in papillary thyroid carcinoma (PTC).Materials and methodsXIST expression was determined in PTC tissues and cell lines by quantitative real-time polymerase chain reaction (PCR) (qRT-PCR). Cellular proliferation, migration, and invasion were measured using the Cell Counting Kit-8 (CCK-8) assay, wound-healing assay, and transwell invasion assay, respectively. Western blotting was used to determine protein expression. The downstream target miRNAs for XIST were identified by luciferase reporter assay and qRT-PCR.ResultsRelative expression of XIST was upregulated in PTC tissues and cell lines. High XIST expression was positively correlated with TNM stage and lymph node metastasis. Function assay demonstrated that knockdown of XIST significantly decreased cell proliferation, migration, and invasion in PTC cells. Moreover, we showed that the effects of XIST on PTC cell progression were mediated by miR-141.ConclusionOur results demonstrated that XIST functioned as an oncogene in PTC progression by regulating miR-141, suggesting that XIST might be a promising therapeutic target for PTC treatment.

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