Literature DB >> 24153116

The tumor suppressing effects of QKI-5 in prostate cancer: a novel diagnostic and prognostic protein.

Yi Zhao1, Gen Zhang2, Mengying Wei3, Xiaozhao Lu3, Hanyan Fu3, Feixue Feng3, Shan Wang3, Wei Lu3, Ning Wu3, Zifan Lu3, Jianlin Yuan2.   

Abstract

In recent years, the RNA-binding protein quaking 5 (QKI-5) has been recognized as a novel tumor suppressor in many cancers. To date, no studies have examined the role of QKI-5 in prostate cancer. The present study was designed to elucidate the correlation of QKI-5 expression with the clinical pathological features and prognosis of prostate cancer. In an overwhelming majority of the 184 cases of prostate cancer samples analyzed, the QKI-5 expression was significantly decreased, which was largely due to the high promoter methylation levels. Using lentiviral vectors, we established two stable prostate cancer cell lines with altered QKI-5 expression, including a QKI-5 overexpressing PC3 cell line and a DU145 cell line with knocked-down QKI-5 expression. The effects of the lentiviral-mediated QKI-5 knockdown on the PC3 cells and DU145 cells were assessed by cell growth curves, flow cytometry (FCM), and an invasion assay. The PC3 cells were transplanted into nude mice, and then, the tumor growth curves and TUNEL staining were determined. These results demonstrated that QKI-5 was highly expressed in benign prostatic hyperplasia (BPH) tissues but not in carcinomatous tissues and that QKI-5 effectively inhibited prostate cancer cell proliferation in vitro and in vivo. In addition, the decrease in QKI-5 expression was closely correlated with the prostate cancer Gleason score, poor differentiation, degree of invasion, lymph node metastasis, distant metastasis, TNM grading, and poor survival. These results indicate that the QKI-5 expression may be a novel, independent factor in the prognosis of prostate cancer patients.

Entities:  

Keywords:  RNA binding protein QKI-5; inhibition; lentivirus; methylation; prognosis; prostatic carcinoma; survival

Mesh:

Substances:

Year:  2013        PMID: 24153116      PMCID: PMC3938513          DOI: 10.4161/cbt.26722

Source DB:  PubMed          Journal:  Cancer Biol Ther        ISSN: 1538-4047            Impact factor:   4.742


  20 in total

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  32 in total

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10.  NF-κB induces miR-148a to sustain TGF-β/Smad signaling activation in glioblastoma.

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