Aberrant Expression Of RNA Binding Protein QKI In Prostate Cancer And Its Tumor Suppressing Effects

Prostate cancer (PCa) is the most common noncutaneous cancer and is thesecond and third cause of cancer death in men in America and Europe. Moreover,prostate cancer is becoming more and more common in China[11]. At present the maintreatment is surgical treatment, while secondary radiotherapy and chemotherapy, butpatients benefit from limited, and because of early prostate cancer with no obvioussymptoms, so many patients are diagnosed when they often have lost the best timingof surgery. Break through the limitations of traditional treatment for prostate cancerpatients that was become an urgent problem. With the progress of gene therapytechniques in molecular biology has been increasingly utilized in clinical diagnosisand treatment of disease, and the targeting characteristics of slight trauma cansignificantly improve the limitations of existing treatments, and thus explore moreprostate cancer-related genes, genes for targeted therapy undertaken become a newdirection for the treatment of prostate cancer.Today, RNA-binding protein and miRNA has been shown in cell biology is akey regulator of points in the post-transcriptional regulation of RNA stability,transcription efficiency, transport and shear. mRNA was also confirmed by the absence of regulation, and is closely related to many human diseases, including cancer.RNA binding protein of QKI family belongs STAR (evolutionarily conserved signaltransduction and activation of RNA family) is an important post-transcriptionalregulatory factors. QKI by identifying and binding to the mRNA3’UTR QKI responseelement (QRE, mainly contains the sequence characteristics NACUAAY-N(1-20)-UAAY a), to adjust the positioning of the target mRNA in the cell, the stabilityand translation efficiency etc, involved in the regulation of the body’s physiologicaland pathological processes. Recent studies have shown that, QKI abnormal expressionof many human tumors and the development of related. In short, all of which pointedQKI inhibition in a variety of tumors.Our study is the first reported case of RNA-binding protein QKI expression inprostate cancer, but the role of QKI first reported in prostate cancer developmentplayed. Byimmunohistochemistry, Western blot and qPCR screening methods QKIexpression levels in tissue samples and pathological expression trend. By screeningfor prostate cancer cell lines, select the Lentiviral overexpression and gene silencingof QKI lentiviral expression levels were adjusted again and the control group forcomparison on the biological function of the cells. QKI in orderto elaborate thedevelopment of prostate cancer in the course of the role played by its mechanism.Specific experiment was divided into the following two parts:1) RNA binding protein QKI expression profiling in prostate cancer tissuesThrough experiments on prostate cancer tissue specimens by imm-uneohist-ochemistry, qPCR and western blot detection method to detect prostatecancer was found in QKI expression level is lower than adjacent control tissue, andwith the level of expression continued to reduce the degree of differentiation of QKIalso showed reduced state.2) To explore the role of QKI RNA binding proteins in prostate cancer and itsmechanismSelect a common three experimental prostate cancer cell lines PC3, DU145,LNCaP cells and this three cell lines were screened expression levels of QKI, It willselect the lowest level of expression QKI used PC3cells expressing lentivirus infection, the relatively high level of expression DU145cells infected with lentivirusgene silencing and stable infected cell lines were constructed. After the success of ourcell model constructed by MTT, plate cloning experiments on stably transfected celllines proliferation tested and found QKI can significantly inhibit prostate cancer cellproliferation (P <0.05). Followed by flow cytometry for cell cycle and apoptosis weredetected and found QKI can make prostate cancer cells in G1phase arrest occurs,reducing the cell into the S phase, while at the same time there has been an increaseexponentially early apoptotic (P <0.01). In cell invasion by Transwell experimentexperiments we found that compared with the control group to speak QKI cansignificantly block cell invasion (P <0.05). Finally, we have to verify the results of theexperiment the cells were further animal experiments, the mice were randomizedsubcutaneously QKI stably transfected cell lines, through the detection of tumorvolume, tumor weight and growth curve plotted found QKI can significantly inhibittumor growth. In the TUNEL assay QKI overexpression of tumor-bearing nude miceorganizations can significantly increase tumor apoptosis (P <0.05).In summary, this study is the first report of domestic RNA-binding protein QKIrole in prostate cancer. The experimental results obtained demonstrate the role of theearly studies QKI prediction of prostate cancer, RNA binding protein inhibits theproliferation of transcriptional level of prostate cancer, prostate cancer and cyclearrest occurs, resulting in apoptosis rising levels. Therefore, we believe QKI fortargeting prostate cancer research is significant.