Cell Line, Tumor ; Genetic Vectors ; Humans ; Male ; Neuraminidase ; genetics ; metabolism ; Prostate ; metabolism ; Prostatic Neoplasms ; metabolism ; pathology

Prostate cancer (PCa) is one of the most common malignancies in the urinary system of males. A growing number of studies have shown that microRNAs, as small ribonucleic acid molecules and a class of non-coding small RNAs, are closely related with PCa and a variety of microRNAs are abnormally expressed in it. This article focuses on the roles of microRNAs in the occurrence and progression of PCa, with a description of differentially expressed microRNAs in PCa and an analysis of their association with its prognosis as well as their correlation with chemotherapy, androgen receptors, and metastasis of PCa.
Disease Progression ; Humans ; Male ; MicroRNAs ; metabolism ; Prognosis ; Prostatic Neoplasms ; chemistry ; genetics ; metabolism ; Receptors, Androgen ; metabolism

OBJECTIVETo explore the mechanism of miR-124 inhibiting the proliferative activity of prostate cancer PC3 cells.

METHODSLuciferase reporter gene assay was used to examine the specific binding ability of miR-124 to PKM2 mRNA 3'-UTR. After miR-124 was transfected mimic to PC3 cells, the expression levels of PKM2 mRNA and protein were detected by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot, respectively. The effects of miR-124 mimic and PKM2 siRNA on the proliferative activity of the PC3 cells were determined by MTT assay.

RESULTSThe expressions of PKM2 mRNA and protein were upregulated (5.12 +/- 0.35) times and (4.05 +/- 0.20) times respectively in the PC3 cells as compared with those in the RWPE-1 cells (P < 0.05). Luciferase reporter gene assay demonstrated that miR-124 targeted PKM2 3'-UTR. At 24 hours after transfection with miR-124 mimic, the PKM2 protein expression in the PC3 cells was downregulated (0.16 +/- 0.04) times (P < 0.05), while the PKM2 mRNA level was not changed significantly (P > 0.05), as compared with the control group. MTT assay showed that both miRNA-124 mimic and PKM2 siRNA could inhibit the proliferation of the PC3 cells, but the former exhibited a greater inhibitory effect than the latter. After transfection with miR-124 mimic and PKM2 siRNA, the cell growth rates were (66.20 +/- 5.10)% vs (82.10 +/- 6.35)% at 24 hours (P < 0.05) and (49.34 +/- 2.37)% vs (70.10 +/- 5.80)% at 48 hours (P < 0.05).

CONCLUSIONmiR-124 can suppress the proliferation of PC3 cells by regulating the PKM2 gene.

Carrier Proteins ; genetics ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; genetics ; Humans ; Male ; Membrane Proteins ; genetics ; metabolism ; MicroRNAs ; genetics ; Prostatic Neoplasms ; genetics ; metabolism ; pathology ; Thyroid Hormones ; genetics ; metabolism ; Transfection

Animals ; Antigens, Neoplasm ; genetics ; metabolism ; Biomarkers, Tumor ; genetics ; metabolism ; Brain Neoplasms ; metabolism ; Cell Adhesion Molecules ; genetics ; metabolism ; Digestive System Neoplasms ; metabolism ; Female ; Genital Neoplasms, Female ; metabolism ; Glioma ; metabolism ; Head and Neck Neoplasms ; metabolism ; Humans ; Immunotherapy ; Male ; Prostatic Neoplasms ; metabolism ; Signal Transduction

Carcinoma ; genetics ; metabolism ; pathology ; surgery ; China ; Humans ; Male ; Oncogene Proteins, Fusion ; genetics ; Prostatic Hyperplasia ; genetics ; metabolism ; pathology ; surgery ; Prostatic Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Proto-Oncogene Proteins c-ets ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Serine Endopeptidases ; genetics ; metabolism

OBJECTIVETo investigate the role of the epigenetic inactivation of Ras association domain family 2 (RASSF2) in the occurrence and development of prostate cancer by detecting the methylation and protein expression of RASSF2 in the tissues of prostate cancer and prostatic hyperplasia.

METHODSWe obtained genome DNA from 30 formalin-fixed paraffin-embedded specimens of prostate cancer (experimental group) and another 30 of prostatic hyperplasia (control group). We detected the methylation of RASSF2 by methylation-specific PCR (MSP) and its protein expression by immunohistochemistry.

RESULTSThe rates of RASSF2 promoter hypermethylation and the absence of its protein expression were 66.7% (20/30) and 70.0% (21/30) respectively in the experimental group, significantly higher than 6.7% (2/30) and 3.3% (1/30) in the control group (P < 0.05). The promoter hypermethylation of RASSF2 was significantly correlated with the absence of its protein expression (P < 0.05).

CONCLUSIONThe epigenetic inactivation of RASSF2 is involved in the occurrence of prostate cancer, and is expected to be a target of molecular diagnosis and treatment of prostate cancer.

DNA Methylation ; Epigenesis, Genetic ; Genes, ras ; Humans ; Male ; Prostatic Neoplasms ; genetics ; metabolism ; Tumor Suppressor Proteins ; genetics ; metabolism

To study the expression of matrix metalloproteinase-2 and -9 in human prostate cancer, matrix metalloproteinase-2 and -9 were immunohistochemically detected in tissues of prostate cancer and benign prostatic hyperplasia (BPH). Our results showed that matrix metalloproteinase-2 and -9 levels in prostate cancer were much higher than those in tissues of BPH, with the cancer invasion being positively correlated with the expression of the metalloproteinases. It is concluded that matrix metalloproteinase-2 and -9 are better molecular markers, which are of help in the diagnosis and prediction of prognosis of prostate cancer.
Humans ; Immunohistochemistry ; Male ; Matrix Metalloproteinase 2 ; biosynthesis ; genetics ; Matrix Metalloproteinase 9 ; biosynthesis ; genetics ; Neoplasm Invasiveness ; Prostatic Hyperplasia ; metabolism ; pathology ; Prostatic Neoplasms ; metabolism ; pathology

OBJECTIVETo detect and analyze the differentially expressed genes in prostate cancer (PCa) and benign prostatic hyperplasia (BPH).

METHODSOligonucleotide microarray containing 465 genes was used to investigate the differentially expressed genes in PCa and BPH.

RESULTSThere were 35 differentially expressed genes between PCa and BPH, of which 17 were up-regulated and 18 down-regulated in PCa.

CONCLUSIONThe study of the differentially expressed genes in PCa and BPH should help to understand the molecular mechanism of PCa and identify the markers for diagnostic and therapeutic use.

Down-Regulation ; Gene Expression Profiling ; Humans ; Male ; Oligonucleotide Array Sequence Analysis ; Prostatic Hyperplasia ; genetics ; metabolism ; Prostatic Neoplasms ; genetics ; metabolism ; Up-Regulation

OBJECTIVETo identify the differential expressions of serum cytokines between prostate cancer (PCa) and benign prostatic hyperplasia (BPH), and provide proteomic evidence for the early diagnosis of PCa.

METHODSWe used human cytokine array to determine the profiles of the serum cytokines obtained from 6 PCa and 6 BPH patients with the PSA level within the grey scale of 4 - 10 ng/ml.

RESULTSWe identified 19 differentially expressed cytokines in the PCa patients, 16 obviously up-regulated, including IL-3, IL-6 and IL-16, and 3 markedly down-regulated, which were Fas/TNFRSF6, TRALR-3 and IGFBP-6. Most of them were involved in such cellular bioprocesses as transcription, proliferation, signal transduction, and apoptosis.

CONCLUSIONThe cytokine antibody assay permits simultaneous measurement of multiple markers in a small volume of serum, and can identify a panel of key cytokines related to the malignant biological behavior of cancer cells. And it helps to find the biomarkers for the early diagnosis, efficacy assessment and prognosis of prostate cancer.

Aged ; Humans ; Interleukin-16 ; blood ; Interleukin-3 ; blood ; Interleukin-6 ; blood ; Male ; Middle Aged ; Prostatic Hyperplasia ; blood ; genetics ; metabolism ; Prostatic Neoplasms ; blood ; genetics ; metabolism ; Proteomics

OBJECTIVETo search for a new method of screening for molecular targets for androgen-dependent prostate cancer.

METHODSWe collected tissue samples and paired serum samples from 3 cases of androgen-dependent prostate cancer (ADPC) treated by surgical resection, and included another 3 samples of benign prostatic hyperplasia (BPH) tissue and normal human serum in the control group. The total proteins extracted were separated and transmembrane by two-dimensional gel electrophoresis, followed by hybridization with the sera of the patients with ADPC and those with hormone-independent prostate cancer (HIPC) as the primary antibodies. The differentially expressed proteins were compared by Western blot, analyzed by MALDI-TOF-MS mass spectrography, and verified by RT-PCR and Western blot following bioinformatic identification.

RESULTSThis modified method exhibited a significantly better effect in displaying differentially expressed proteins, by which 12 differentially expressed protein spots were identified, including Beclin1, glutathione S-transferase P (GSTP1-1), ZBTB7, dihydrodiol dehydrogenase 2 (DDH), enolase (ENO1), glucose-dependent insulin-releasing peptide receptor (GIPR), Mn-superoxide dismutase (MnSOD), phosphoglycerate mutase 1 (PGAM1), amino-peptidyl-prolyl cistrons isomerase (PPIA), and phospholipid-PE-binding protein (PEBP). The mRNA and protein expressions of Beclin1 were significantly down-regulated in androgen-dependent prostate cancer tissues.

CONCLUSIONThis modified serum-guided immunoblotting technique has provided a new method for clarifying the molecular mechanisms of the occurrence and progression of HIPC, in which Beclin1-mediated autophagy may play a key role.

Biomarkers, Tumor ; blood ; Blotting, Western ; Humans ; Immunoblotting ; methods ; Male ; Mass Spectrometry ; Prostatic Neoplasms ; genetics ; metabolism ; Proteomics