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10.3892/or.2016.4791

http://scihub22266oqcxt.onion/10.3892/or.2016.4791
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C4899005!4899005 !27176634
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suck abstract from ncbi

pmid27176634
      Oncol+Rep 2016 ; 36 (1 ): 10-22
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  • Long non-coding RNA ATB promotes growth and epithelial-mesenchymal transition and predicts poor prognosis in human prostate carcinoma #MMPMID27176634
  • Xu S ; Yi XM ; Tang CP ; Ge JP ; Zhang ZY ; Zhou WQ
  • Oncol Rep 2016[Jul]; 36 (1 ): 10-22 PMID27176634 show ga
  • Long non-coding RNAs (lncRNAs) have been identified to be critical mediators in various tumors associated with cancer progression. Long non-coding RNA activated by TGF-? (lncRNA-ATB) is a stimulator of epithelial-mesenchymal transition (EMT) and serves as a novel prognostic biomarker for hepatocellular carcinoma. However, the biological role and clinical significance of lncRNA-ATB in human prostate cancer have yet to be fully elucidated. The present study was designed to explore the expression of lncRNA-ATB in human prostate cancer patients and the role of lncRNA-ATB in prostate cancer cells. We showed that lncRNA-ATB expression was significantly upregulated in tumor tissues in patients with prostate cancer in comparison with adjacent non-tumor tissues. Further analysis indicted that high lncRNA-ATB expression may be an independent prognostic factor for biochemical recurrence (BCR)-free survival in prostate cancer patients. Overexpression of lncRNA-ATB promoted, and knockdown of lncRNA-ATB inhibited the growth of prostate cancer cells via regulations of cell cycle regulatory protein expression levels. In addition, lncRNA-ATB stimulated epithelial-mesenchymal transition (EMT) associated with ZEB1 and ZNF217 expression levels via ERK and PI3K/AKT signaling pathways. These results indicated that lncRNA-ATB may be considered as a new predictor in the clinical prognosis of patients with prostate cancer. Overexpression of lncRNA-ATB exerts mitogenic and EMT effects of prostate cancer via activation of ERK and PI3K/AKT signaling pathways.
  • |Cadherins/biosynthesis [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation/genetics [MESH]
  • |Cyclin D1/biosynthesis [MESH]
  • |Cyclin E/biosynthesis [MESH]
  • |Epithelial-Mesenchymal Transition/*genetics [MESH]
  • |Extracellular Signal-Regulated MAP Kinases/*metabolism [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Humans [MESH]
  • |Male [MESH]
  • |Neoplasm Invasiveness/genetics [MESH]
  • |Oncogene Proteins/biosynthesis [MESH]
  • |Phosphatidylinositol 3-Kinases/*metabolism [MESH]
  • |Prostatic Neoplasms/genetics/mortality/*pathology/therapy [MESH]
  • |Proto-Oncogene Proteins c-akt/*metabolism [MESH]
  • |RNA Interference [MESH]
  • |RNA, Long Noncoding/*genetics [MESH]
  • |RNA, Small Interfering/genetics [MESH]
  • |Signal Transduction/genetics [MESH]
  • |Trans-Activators/biosynthesis [MESH]
  • |Vimentin/biosynthesis [MESH]
  • |Zinc Finger E-box-Binding Homeobox 1/biosynthesis [MESH]


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