PCSEAT

Last update 08 May 2025

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Synonyms

PCSEAT, PRCAT38, prostate cancer expressed EZH2 associated transcript

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100 Clinical Results associated with PCSEAT

100 Translational Medicine associated with PCSEAT

0 Patents (Medical) associated with PCSEAT

Literatures (Medical) associated with PCSEAT

01 Aug 2018·The ProstateQ3 · MEDICINE

Two long non‐coding RNAs, Prcat17.3 and Prcat38, could efficiently discriminate benign prostate hyperplasia from prostate cancer

Q3 · MEDICINE

Article

Author: Bayat, Hamid ; Ziaee, Seyed‐Amir Mohsen ; Narouie, Behzad ; Mowla, Seyed Javad

BackgroundLong non‐coding RNAs (lncRNAs) have recently appeared as new players in cancer biology. Recently, a number of new prostate cancer‐associated lncRNAs has been listed via RNA‐seq approach by Mitranscriptome project. By analyzing this data we chose four lncRNAs (Prcat17.3, Prcat38, Prcat47, and Cat2184.4) and evaluated their expressions and their abilities to discriminate prostate tumors from benign prostate hyperplasia (BPH).MethodsFresh Prostate tissue samples (30 BPH, and 30 tumor samples) and urine samples (19 BPH, and 19 tumor samples) were collected and their total RNA extracted for cDNA syntheses. The expression of candidate lncRNAs was assessed by the real‐time PCR technique.ResultsOur data revealed that the expression levels of PRCAT17.3 (P < 0.0001) and PRCAT38 (P < 0.0002) were significantly upregulated in human prostate cancer tissues, compared to BPH ones. Moreover, the altered expression was much higher for PRCAT17.3 (∼2000 folds) than PRCAT38 (∼50 folds). In contrast, the expression of Cat2184.4 showed a significant down‐regulation in tumor samples (P < 0.0001), compared to BPH ones. While the expression level of PRCAT47 was increased in cancer samples, the changes were not statistically significant. In discriminating prostate tumors from BPH samples, Prcat17.3 (AUC‐ROC, 0.927) demonstrated a better diagnostic efficacy than Prcat38 (AUC‐ROC, 0.778). Moreover, real‐time RT‐PCR analyses on urine samples of prostate cancer patients revealed that prcat17.3 level is significantly elevated, (P < 0.0197; AUC‐ROC value of 0.72), compared to that of BPH patients.ConclusionWe introduce here two novel lncRNAs with a potential application in diagnosis of prostate cancer.

01 Jul 2018·Biochemical and Biophysical Research CommunicationsQ3 · BIOLOGY

The long non-coding RNA PCSEAT exhibits an oncogenic property in prostate cancer and functions as a competing endogenous RNA that associates with EZH2

Q3 · BIOLOGY

Article

Author: Gao, Shan ; Gu, Yinmin ; Li, Rong ; Xiaohui Yang ; Yang, Xiaohui ; Huang, Kuohsiang ; Cheng, Tianyou ; Liu, Siying ; Wang, Liang ; Yuan, Yi ; Zhao, Yuhui ; Song, Dalong

Prostate cancer (PCa) is the most common malignancy and the leading cause of cancer deaths in males. Recent studies demonstrate that long non-coding RNAs (lncRNAs) are involved in many aspects of PCa. However, their biological roles in PCa remain imperfectly understood. Here,wecharacterized anlncRNA, PCaspecific expression and EZH2-associatedtranscript (PCSEAT, annotated as PRCAT38), which is specifically overexpressedin PCa. We further demonstrated that knockdown of PCSEAT results in the reduction of PCa cell growth and motility, and overexpression of PCSEAT reverses these phenotypes. Furthermore, bioactive PCSEAT is incorporated into exosomes and transmitted to adjacent cells, thus promoting cell proliferation and motility. Mechanistically, we found that PCSEAT promotes cell proliferation, at least in part by affecting miR-143-3p- and miR-24-2-5p-mediated regulation of EZH2, suggesting that PCSEAT and EZH2 competitively 'sponge' miR-143-3p and miR-24-2-5p.Overall, ourresultsrevealthat PCSEAT is specifically overexpressed in PCa patients and a potential oncogene in PCa cells via mediating EZH2 activity, indicating that PCSEAT may be a potential therapeutic target in PCa.

CellsQ3 · BIOLOGY

Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer

Q3 · BIOLOGY

ArticleOA

Author: Su, Ting ; Chen, Zikai ; Tang, Chang ; Li, Qidong ; Guo, Tangfei ; Liang, Bin ; Chang, Xiaolan ; Xie, Lingzhu ; Song, Xuhong ; Huang, Dongyang

Prostate cancer is a common carcinoma in males, the development of which involves the androgen receptor (AR) as a key regulator. AR transactivation induces the high expression of androgen-regulated genes, including transmembrane protease serine 2 (TMPRSS2) and long noncoding RNA prostate cancer-associated transcript 38 (PRCAT38). PRCAT38 and TMPRSS2 are both located on chromosome 21, separated by a series of enhancers. PRCAT38 is a prostate-specific long noncoding RNA that is highly expressed in cancer tissue as compared to normal tissue. Here, we show chromatin looping by enhancers E1 and E2 with the promoters for PRCAT38 and TMPRSS2, indicating the co-regulation of PRCAT38 and TMPRSS2 by the same enhancers. The knockout of enhancer E1 or E2 simultaneously impaired the transcription of PRCAT38 and TMPRSS2 and inhibited cell growth and migration. Moreover, the loop formation and enhancer activity were mediated by AR/FOXA1 binding and the activity of acetyltransferase p300. Our findings demonstrate the utilization of shared enhancers in the joint regulation of two oncogenes in prostate cancer cells.

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