The prognostic value of lncRNA, YAP, and EGR-1 gene expression was evaluated using the online database Gene Expression Profiling Interactive Analysis (GEPIA; http://gepia.cancer-pku.cn) and Kaplan-Meier Plotter (www.kmplot.com), respectively. 17. wound healing, Transwell, and tumor growth inhibition study in vivo. The clinical associations of LINC01508 in OC were evaluated using correlation analysis. The effects of verteporfin (VP) on cisplatin were explored to reveal the function of the hippo-YAP pathway on the cisplatin tolerance of C13K. Results LINC01508 was downregulated in cisplatin-resistant OC cells and platinum-resistant OC tissue 20-HETE (p 0.01). LINC01508 downregulation was correlated with tumor size, residual tumor, and platinum resistance. The overexpression of LINC01508 improves in vitro and in vivo sensitivity to cisplatin while predicts the poor overall survival which need further follow-up research. The increased level of LINC01508 could suppress the cisplatin resistance of OC cells through the inhibition of the hippo-YAP pathway. Conclusions The study proposes that dysregulation of LINC01508 expression results in resistance of OC to cisplatin through the inhibition of the hippo-YAP pathway. strong class=”kwd-title” Keywords: Ovarian Cancer, Long Non-Coding RNA “type”:”entrez-nucleotide”,”attrs”:”text”:”C01508″,”term_id”:”1433738″,”term_text”:”C01508″C01508, Hippo/YAP Signaling Pathway, Cisplatin- Resistance INTRODUCTION Ovarian cancer (OC) is the most lethal gynecological malignancy afflicting women with a high incidence of recurrence. The cytotoxic-based platinum compound cisplatin has been commonly used in OC treatment for almost three decades [1]. However, the intrinsic and acquired resistance to cisplatin in cancer cells remains a big challenge for overall survival (OS) [2]. It is important to understand the new mechanism(s) of cisplatin resistance and develop new strategies for OC treatments. Long non-coding RNAs (lncRNAs) are defined as RNA transcripts comprising more than 200 nucleotides. Most of them are incapable of encoding proteins, which are significantly different from micro RNAs (miRNAs), and small RNAs (siRNAs) [3,4]. Recent data shed light on the numerous and indispensable functions of non-coding RNAs (ncRNAs), particularly in carcinogenesis and chemo-resistance lncRNAs [5,6,7]. lncRNAs may be superior biomarkers in cancer. It is a new area of molecular biology and may have better specificity [8,9,10]. Until recently, only a few human lncRNAs have been demonstrated to contribute to acquired resistance. A study published by Ouyang et al. [11] showed that LINC01508 is a potential biomarker for predicting breast cancer response to neoadjuvant chemotherapy (NAC). Furthermore, this is the only report on the relationship between LINC01508 and cancer. LINC01508 is located on chromosome 9q22.2 with 1,030 nt in length. As a new lncRNA, the expression patterns of LINC1508 and its clinical 20-HETE significance in OC remain uncertain. It is essential to analyze the dysregulated expressed 20-HETE LINC01508 in OC and clarify its regulatory function in developing resistance to therapy. The current study was conducted to aim at the LINC01508 expression in OC and analyze its potential associations with clinicopathological characteristics and platinum resistance in vitro and in vivo. In conclusion, our study might provide a novel mechanism and potential therapeutic target for cisplatin resistance OC. MATERIALS AND METHODS 1. Microarrays and computational analysis The Arraystar Human LncRNA microarray used for the microarray screening number was v4.0. Differentially expressed genes were selected by the R programming language. LncRNA expression scatters profiling (fold change 2.0; p 0.05) between OV2008 and C13K cells was performed to identify significantly different expressions of lncRNAs. 2. Patients and tissue specimens The study protocol was approved by the Medical Ethics Committee of the First Affiliated Hospital of Anhui Medical University, China. Informed consent was obtained from 2017 to 20-HETE 2019. A total of 71 specimens of serous ovarian cancer, 25 ovarian serous 20-HETE cystadenomas, and 19 normal ovarian epithelium tissues from benign tumor patients were included for study. OC patients ages were 36C75 years old (mean age, 48.42 years). Thirteen cases were stage ICII, and 58 cases were stage IIICIV. Histopathology and tumor grade were determined via pathology. None of the patients had been subjected to chemotherapy or radiotherapy before surgery. All were treated with systemic platinum-based chemotherapy following surgery. According to the International Federation of Gynecology and Obstetrics (FIGO) staging system, the tumor stage was determined. For experiments on platinum-based chemotherapy resistance, patients with OC were divided into two groups (platinum-resistant and platinum-sensitive) according to the criteria described below. Patient response to chemotherapy was evaluated according to National Comprehensive Cancer Network guidelines (version 1.2017, ovarian cancer). The guideline has divided sensitive from resistant disease at six months [12]. Rabbit Polyclonal to STK17B 3. Cell line and cell culture The cisplatin-sensitive human ovarian cancer cell lines OV2008 and its cisplatin-resistant clone C13K were supplied by Dr. Wen-cheng Ding (Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology). The human.