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      Long non-coding RNA TMPO-AS1 serves as a tumor promoter in pancreatic carcinoma by regulating miR-383-5p/SOX11

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          Abstract

          The dysregulation of lncRNA TMPO antisense RNA 1 (TMPO-AS1) has been detected in various malignant tumors. However, the role of lncRNA TMPO-AS1 remains unclear in pancreatic carcinoma. The present study aimed to elucidate the functional mechanism of TMPO-AS1 in pancreatic carcinoma. In the present study, RT-qPCR, western blotting, MTT, Transwell, luciferase reporter and xenograft assays were used to investigate the role of lncRNA TMPO-AS1 in pancreatic carcinoma. Upregulation of lncRNA TMPO-AS1 was revealed in pancreatic carcinoma tissues and cells. Furthermore, knockdown of TMPO-AS1 restrained cell proliferation and motility in pancreatic carcinoma. In addition, microRNA (miR)-383-5p acted as a ‘sponge’ for lncRNA TMPO-AS1. The expression levels of lncRNA TMPO-AS1 and miR-383-5p were mutually inhibited in pancreatic carcinoma. Moreover, miR-383-5p was revealed to directly target SRY-related high-mobility group box 11 (SOX11). Notably, SOX11 could promote the occurrence of pancreatic carcinoma by interacting with the lncRNA TMPO-AS1/miR-383-5p axis. In conclusion, upregulation of lncRNA TMPO-AS1 promoted tumor growth, cell migration and invasion in pancreatic carcinoma by downregulating miR-383-5p and upregulating SOX11.

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          Most cited references 26

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          Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method.

          The two most commonly used methods to analyze data from real-time, quantitative PCR experiments are absolute quantification and relative quantification. Absolute quantification determines the input copy number, usually by relating the PCR signal to a standard curve. Relative quantification relates the PCR signal of the target transcript in a treatment group to that of another sample such as an untreated control. The 2(-Delta Delta C(T)) method is a convenient way to analyze the relative changes in gene expression from real-time quantitative PCR experiments. The purpose of this report is to present the derivation, assumptions, and applications of the 2(-Delta Delta C(T)) method. In addition, we present the derivation and applications of two variations of the 2(-Delta Delta C(T)) method that may be useful in the analysis of real-time, quantitative PCR data. Copyright 2001 Elsevier Science (USA).
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            Recent progress in pancreatic cancer.

            Pancreatic cancer is currently one of the deadliest of the solid malignancies. However, surgery to resect neoplasms of the pancreas is safer and less invasive than ever, novel drug combinations have been shown to improve survival, advances in radiation therapy have resulted in less toxicity, and enormous strides have been made in the understanding of the fundamental genetics of pancreatic cancer. These advances provide hope but they also increase the complexity of caring for patients. It is clear that multidisciplinary care that provides comprehensive and coordinated evaluation and treatment is the most effective way to manage patients with pancreatic cancer. Copyright © 2013 American Cancer Society, Inc.
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              LncRNA-PVT1 promotes pancreatic cancer cells proliferation and migration through acting as a molecular sponge to regulate miR-448.

              The identification and characterization of long non-coding RNAs (lncRNAs) in diverse biological process has currently developed rapidly. LncRNA-PVT1, located adjacent to the MYC locus on chromosomal region 8q24, has been reported to be associated with many biological processes. However, the function and mechanism of PVT1 in pancreatic carcinoma (PC) is poorly understood. In this present study, we first measured the level of PVT1 in the PC cell lines and tissues by quantitative real-time PCR (qRT-PCR), and then employed loss-of-function and gain-of-function approaches to explore the association between PVT1 expression levels and PC cell proliferation/migration ability. Furthermore, bioinformatics analysis was utilized to show that PVT1 contains binding site for miR-448 and an inverse correlation between PVT1 and miR-448 was obtained in PC specimens. Additionally, dual luciferase reporter assay, RNA-binding protein immunoprecipitation (RIP) and applied biotin-avidin pulldown system were applied to further confirm that PVT1 directly bind with microRNA binding site harboring in the PVT1 sequence. Then, SERBP1 was identified as a target of miR-448 according to the gene expression array analysis of PC clinical samples. Together, we revealed that PVT1 functions as an endogenous "sponge" by competing for miR-448 binding to regulate the miRNA target SERBP1 and, therefore, promotes the proliferation and migration of PC cells.
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                Author and article information

                Journal
                Oncol Lett
                Oncol Lett
                OL
                Oncology Letters
                D.A. Spandidos
                1792-1074
                1792-1082
                April 2021
                04 February 2021
                04 February 2021
                : 21
                : 4
                Affiliations
                [1 ]Department of General Surgery, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), Qingdao, Shandong 266000, P.R. China
                [2 ]Department of Oncology, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), Qingdao, Shandong 266000, P.R. China
                Author notes
                Correspondence to: Dr Ting Zhao, Department of General Surgery, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), 4 Renmin Road, Qingdao, Shandong 266000, P.R. China, E-mail: dmy081031@ 123456163.com
                Article
                OL-0-0-12517
                10.3892/ol.2021.12517
                7882873
                Copyright: © Xue et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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