Circulating miRNA-141 as a non-invasive biomarker for prostate cancer detection and prognosis

AIM:To analyze circulating miR-141 in the serum as a non-invasive biomarker in the patients with prostate cancer (PCa) and benign prostate hyperplasia (BPH), and healthy individuals. METHODS:A total of 75 patients with PCa, 52 with BPH and 40 healthy individuals were enrolled into this study. Total RNA was isolated from the serum samples and the circulating levels of miR-141 were determined using quantitative real-time polymerase chain reaction. RESULTS:The serum levels of miR-141 were significantly higher in the patients with PCa compared to the patients with BPH and the healthy controls (P<0.01). The level of miR-141 in PCa group obviously differed from that in BPH group and healthy control group with high diagnosis performance, with areas under the curve of 0.785 and 0.801, respectively. No statistically significant difference of the serum miR-141 levels between the patients with BPH and healthy individuals was observed (P>0.05). The serum miR-141 level was also found to be related to Gleason score, clinical stage and bone metastasis status of the patients with PCa (P<0.05), and the patients with higher Gleason scores had higher serum miR-141 levels. No relationship was detected between miRNA-141 level and the patient’s age, biochemistry recurrence and serum prostate-specific antigen level (P>0.05 for all comparisons). CONCLUSION: Circulating miR-141 could serve as a non-invasive biomarker for prostate cancer diagnosis, staging and prognosis prediction.     

Relationship between phosphoglycerate kinase 1 and clinical features of prostate cancer and its role in prognosis

AIM: To study the expression and prognostic functions of phosphoglycerate kinase 1 (PGK1) in prostate cancer. METHODS: The prostatic samples were collected from the patients with prostate cancer and benign prostatic hyperplasia (BPH) in TCM-Integrated Hospital of Southern Medical University from Jan 2013 to Dec 2013. The protein expression of PGK1 in the prostate specimens was detected by immunohistochemical analysis and Western blot. Furthermore, the correlations of PGK1 expression with the clinicopathological features and prognosis of prostate cancer were also evaluate. RESULTS: The expression of PGK1 in the prostate specimens was significantly up-regulated compared with the BPH individuals. In addition, the expression of PGK1 was significantly correlated with the local infiltration, Gleason score, TNM grade, bone metastasis, and serum prostate-specific antigen (PSA) concentration. Finally, bone metastasis, serum PSA level and PGK1 expression were independent risk factors for prostate cancer illustrated by Cox analysis, and high expression of PGK1 was correlated with poor prognosis. CONCLUSION: PGK1 expression is an independent risk factor for prostate cancer, and it might act as a prognostic biomarker for prostate cancer.     

Value of endonuclease domain containing 1 in progression of prostate cancer

AIM: To analyze the difference of endonuclease domain containing 1 (ENDOD1) expression between benign prostatic hyperplasia (BPH) tissues and prostate cancer (PCa) tissues and to investigate the effect of ENDOD1 on the biological function of human prostate cancer cells. METHODS: The BPH samples (n=20) and PCa samples (n=21) were processed and analyzed according to the instruction of immunohistochemical (IHC) staining. The mRNA and protein levels of ENDOD1 in the normal prostate epithelial cells and prostate cancer cells were evaluated by RT-qPCR and Western blot, respectively. The recombinant plasmids pCMV-N-Flag-ENDOD1 was constructed and was transfected into the human prostate cancer cells. The proliferation, apoptosis, migration and invasion abilities of the prostate cancer cells were evaluated by MTT assay, flow cytometry, Transwell migration and Matrigel invasion assays, respectively. RESULTS: The analysis of variance of the immunoreactivity score showed that PCa tissues with high Gleason score displayed significantly lower ENDOD1expression than that with low Gleason score and BPH (P<0.05). The expression of ENDOD1 at mRNA and protein levels in PC3 cells and DU145 cells was significantly lower than that in the LNCap cells (P<0.05). The proliferation of DU145 transfected with ENDOD1 was inhibited. The flow cytometry indicated that ENDOD1 over-expression in the DU145 cells resulted in a notable increase in G₀/G₁ phase arrest (P<0.05), but the apoptotic rates showed no statistical difference. The results of Transwell assay showed that migration and invasion abilities of the cells were also inhibited after transfection with over-expressing ENDOD1 plasmid (P<0.05). CONCLUSION: The expression of ENDOD1 significantly decreased in prostate cancer with high Gleaon score. Meanwhile, the ENDOD1 is specifically down-regulated in androgen independent prostate cancer (AIPC) cell lines. Over-expression of ENDOD1 remarkably inhibits the proliferation, migration and invasion abilities of AIPC.     

Expression of SAL-like 4 protein in human prostate cancer tissue/cell lines and its relationship with clinical outcome

AIM:To evaluate the expression of SAL-like 4 (SALL4) protein in human prostate cancer cell lines and tissues, and to analyze the relationship between SALL4 expression and the clinicopathological parameters. METHODS:Immunofluorescence, RT-PCR and Western blotting were performed to detect the expression of SALL4 at mRNA and protein levels in 3 common prostate cancer cell lines LNCaP, DU145 and PC-3. The normal prostate epithelial cell line RWPE-1 was used for control. The protein levels of SALL4 in the tissues of benign prostate hyperplasia and prostate cancer tissues were determined by the method of immunohistochemistry. RESULTS:The SALL4 protein was predominantly expressed in the cytoplasm of the cells. The protein levels of SALL4 in 3 common prostate cancer cell lines were significantly higher than that in RWPE-1 cells. However, the mRNA level of SALL4 had no obvious difference among the 4 cell lines. Immunohistochemistry results showed that the expression level of SALL4 in the cancerous tissues was significantly higher than that in noncancerous (benign and normal) prostatic tissues. In addition, we found that the expression level of SALL4 in prostate cancer was significantly correlated with the Gleason score, clinical stage, prognosis estimation and tissue prostate-specific antigen (PSA) expression, but not associated with age, the level of serum total PSA, prostate volume and the expression of androgen receptor in the tissues of the patients. CONCLUSION: The over-expression of SALL4 protein may play an important role in the pathogenesis and progression of prostate cancer, and provides some reference indexes for estimating the malignancy, progression and prognosis of prostate cancer.     

Progress of c-FLIP overexpression in prostatic carcinoma

Cellular FLICE-inhibitory protein (c-FLIP) is a key anti-apoptotic regulator that inhibits death receptor (DR) signal pathway mediated by suppressing procaspase-8 activation. c-FLIP has been found to be elevated in prostatic carcinoma (PCa), and there is a strong correlation between the overexpression of c-FLIP and PCa. In the present paper, we review the links beteween c-FLIP and androgen receptor (AR) signal pathway, which regulate and promote the survival of androgen-independent prostate cancer (AIPC) and describe the possibility of c-FLIP as a therapeutic target of PCa.     

Antiproliferation effects of 188Re labeled monoclonal antibody on prostate cancer cells in vitro

AIM: To investigate the effect of 188Re labeled monoclonal antibody on prostatic specific membrane antigen 7E11C5.3,radioimmunotherapy for the treatment of human prostate cancer cell line LNCaP in vitro.METHODS: 188Re-7E11C5.3 was prepared by direct 2-mercaptoethanol reduction method.Labeling efficiency and radiochemical purity was measured by paper chromatography.Immunoreactive fraction was determined by linear extrapolation.Cytotoxicity to LNCaP cells was determined by MTT assay.RESULTS: The labeling yield of 188Re-7E11C5.3 was (93.16±2.18)%,the radiochemical purity was (95.62±0.48)%,and the immunoreactive fraction was (74.86±1.86)%.The inhibitory effect of 188Re-7E11C5.3 on cell proliferation of LNCaP cells was significantly higher than that of 188Re-mIgG or 188ReO-4.The 50% inhibitory doses (IC50) of 188Re-7E11C5.3,188Re-mIgG,and 188ReO-4 were (23.38±3.73)×107 Bq/L,(59.21±8.02)×107 Bq/L and (68.89±10.91)×107 Bq/L,respectively.CONCLUSION: 188Re-7E11C5.3 can effectively inhibit the growth of in vitro cultured prostate cancer cells and shows much potential for prostate cancer radioimmunotherapy.     

Study on mutations of exon BH of the androgen receptor gene in 45 cases of patients with prostate cancer

AIM and METHODS: To learn more about the mechanism of prostate cancer (PC) development and progression to androgen independence, the exons BH of the androgen receptor (AR) gene of forty-five patients with prostate cancer, six puncture tissues and thirty-nine slide tissues, were analyzed by polymerase chain reaction-single strand conformation technique (PCR-SSCP). RESULTS: Seven abnormal mobility shifts were found in five patients by PCR-SSCP. Combining the method with direct DNA cycle sequencing, two distinct missense (Glu872Gln, Met886Ile) point mutations were identified in puncture tissues from two patients of advanced prostate cancer with distant metastasis. These two point mutations represented two novel mutations. CONCLUSION: AR gene mutations might play an important role in the development and progression of prostate cancer.     

UV-spectrophotometric screening of 5α-reductase inhibitors for benign prostatic hyperplasia treatment

AIM: Tranditional methods of screening drugs for benign prostatic hyperplasia (BPH) requires senile male animals such as dogs or rats. It consumes a long time to get the results. Over-expression of type Ⅱ5α-reductase in prastate induces BPH. A fast and efficient screening model of type Ⅱ5α-reductase inhibitors for BPH was set up in this paper. METHODS: Microsomes were extracted from male Sprague-Dawley rat livers by gradient centrifugation. Type Ⅱ5α-reductase enzyme-catalyzed reaction was assayed by UV-spectrophotometry using testosterone as a substrate and NADPH as hydrogen donor. The change of enzymatic activity was recorded with a NADPH wavelength of 340 nm by subtracted descending velocity of the control (without 5α-reductase). Effects at different conditions (temperatures, pH, enzyme and testosterone concentrations) on 5α-reductase were assayed. RESULTS: The suitable condition of type Ⅱ5α-reductase reaction was defined as concentration of 109.05 mg protein/L enzyme (pH 6.00) with 2 μmol/L testosterone at 37 ℃. Michaelis constant of type Ⅱ5α-reductase was 0.6 μmol/L. Finasteride, a new drug for BPH, significantly inhibited activity of type Ⅱ5α-reductase. IC50 of finasteride was 64.1 nmol/L. As solvent of drugs, concentration of ethanol below 1.1% did not inhibite enzymatic activity (P>0.05). Concentration of ethanol above 1.6 % could obviously suppress enzymatic activity (P<0.01). Daytime difference within five days had no significant difference (P>0.05). CONCLUSION: A handy and fast screening method for type Ⅱ5α-reductase inhibitors has been set up using UV-spectrophotometry. It may be used to screening drugs for BPH treatment.     

Construction of human prostate-specific membrane antigen expression vector and identification of tissue specificity

AIM: To construct a prostate-specific expression vector of promoter and enhancer of human prostate-specific membrane antigen (PSMA).METHODS: The promoter and enhancer of PSMA were amplified by PCR separately. The two segments were cloned into the expression vector pGL3-Basic, a prostate-specific expression vector pGL3-PSMP-PSME was constructed. The vector was transfected into prostatic carcinoma cell PC-3M and four kinds of non-prostatic carcinoma cells by lipofectamine. The activity of luciferase of transfected cells and tissue specificity of vector was examined at 48 hours after transfection. RESULTS: With DNA sequence of the vector pGL3-PSMP-PSME, the segment of clone was proved correct. The activity of luciferase of the pGL3-PSMP-PSME was expressed distinctly in PC-3M and was not expressed in other nonprostate cell lines. CONCLUSION: The prostate-specific expression vector was constructed successfully. It lays foundation for studying target gene therapy of the prostate cancer.     

Effect of RelB on proteasome inhibitor-induced maspin expression

AIM: To investigate the effects of RelB on proteasome inhibitor-induced maspin expression in prostate cancer cells. METHODS: Western blotting analysis was performed to examine endogenous and proteasome inhibitor(MG-132)-induced expression of RelA, RelB and maspin in prostate cancer cells. The expression profiles of RelB and maspin in human prostate cancer tissues were obtained by immunohistochemistry assay. RNA interference targeting RelB was performed in DU145 cells. The effects of RelB-silencing on maspin expression induced by MG-132 were detected by Western blotting. The cell viability was determined by PI staining and FACS analysis. RESULTS: RelB expression was increased in androgen-independent prostate cancer cell line DU145, while maspin expression was minimally detected. Among 10 tissue samples tested, a strong nuclear RelB staining and an absence of maspin expression were found in high-grade specimens (Gleason scores 4-5). RelB expression was reduced upon treatment with MG-132 for 24 h, which was coincided with the induction of maspin expression. RelB-silencing in DU145 cells by siRNA didn't influence the proteasome inhibitor-induced maspin expression. CONCLUSION: The expression of RelB is inversely correlated to maspin expression in androgen-independent prostate cancer cells and prostate cancer tissues. RelB expression is critical to the proteasome inhibitor-induced maspin expression.     

PSMA activates JNK/SAPK pathway and regulates apoptosis of prostate cancer cells

AIM：To investigate the effects of prostate-specific membrane antigen (PSMA) on the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) pathway and the apoptosis of prostate cancer cells. METHODS：The shRNA lentiviral vector with high efficiency was constructed in the previous study to block the PSMA expression in the prostate cancer cells as experimental interference group, while the constructed vector of PSMA was transfected into the prostate cancer cells to promote PSMA expression as positive experimental group. The control group was the cell line without any treatment. JNK/SAPK inhibitor SP600125 was used as a negative control. Western blotting and immunocytochemistry were used to observe the p-JNK/SAPK expression. The cell growth curve was determined by CCK-8 assay. The cell cycle and apoptosis were analyzed by flow cytometry. RESULTS：Inhibition of PSMA expression resulted in the decrease of p-JNK/SAPK expression levels, while enhancement of the PSMA expression made the increase in the expression of p-JNK/SAPK. SP600125 decreased the level of p-JNK/SAPK, and no significant difference among the 3 groups was observed. The cell proliferation and S-phase percentage decreased after the inhibition of PSMA, while the cells in the 3 groups with SP600125 treatment only had low levels of cell proliferation and percentage of S phase. The inhibition of PSMA promoted apoptosis, while in the enhanced PSMA expression group, apoptotic rate was significantly reduced. After adding SP600125, the cell apoptotic rate was lower than that in normal culture group. CONCLUSION：PSMA has an impact on the proliferation, cell cycle and apoptosis of prostate cancer cells by up-regulating JNK/SAPK signaling pathway, but the JNK/SAPK signaling is not the only path.     

Relationship between STEAP expression and hydrogen peroxide in human prostate tissues

AIM:To observe the STEAP expression and its function in human prostate tissues.METHODS:The expressions of STEAP mRNA and protein were detected by RT-PCR and Western blotting. H₂O₂ and SOD levels were detected by molybdic acid reduction and xanthine oxidation methods respectively.RESULTS:STEAP mRNA and protein were highly expressed in prostate cancer tissues. H₂O₂ and SOD levels in prostate cancer were obviously higher than those in normal prostate tissue.CONCLUSION:The function of STEAP gene is possibly to induce intracellular H₂O₂ and promote cell growth.     

Diagnostic and prognostic application of proteomic patterns in breast cancer

AIM: To detect the serum proteomic patterns in patients of breast cancer by the method of SELDI-TOF-MS and CM10 ProteinChip, and to screen the biomarker candidates, build and validate the diagnostic models, and evaluate its clinical value in surveillance and follow-up after operation. METHODS: The SELDI-TOF-MS technology and CM10 ProteinChip were used to detect the proteomic patterns of serum from 63 breast cancer patients and 40 healthy women. The biomarker candidates were screened and the diagnostic models were constructed by ZJU-PDAS software. Meanwhile, the model was blind-validated in another 23 patients and 20 healthy women. At the same time, 16 serum samples were detected to evaluate its value in surveillance and follow-up after operation. RESULTS: The best model was composed by two protein peaks (BC1/3.9 kD and BC2/5.6 kD) with its sensitivity and specificity of 87.30% (55/63) and 95.00% (38/40), respectively. The sensitivity and specificity in the blind-validation of new cases were 95.65% (22/23) and 85.00% (17/20), respectively. The diagnostic efficacies were the same to the patients of different stages (P>0.05). The expression of BC1 increased while BC2 decreased after operation. The expression of BC2 in the patients with recurrence or metastasis was higher than that in the tumor-free survivors (P<0.05). CONCLUSION: This method shows its potential in detection, surveillance and follow-up after operation. The method is also useful for screening the novel and better biomarkers in breast cancer.     

Changes of cellular immunological function after surgical operation in patients with locally advanced lung cancer

AIM: To study the change of cellular immunological function in patients with locally advanced lung cancer before and after operations. METHODS: A lung cancer group of 20 cases with locally advanced lung cancer (group A), a benign disease group of 20 cases with lung benign disease (group B) and a normal group of 20 cases from healthy volunteers (group C) were set up. The levels of the peripheral blood T lymphocyte subsets (CD+3, CD+4, CD+8, CD+4/ CD+8 ratio) were detected in the group A before operation and on the 10th day and 17th day after operation by indirect immuno-fluorescence assay and contrasted with the group B and group C. RESULTS: The levels of T lymphocyte subsets in group A were abnormal before operation, CD+3, CD+4/ CD+8 ratio were significantly lower than those in group B and group C (P<0.05), and CD+8 was significantly higher (P<0.05). CD+3 significantly increased (P<0.05) and CD+8 decreased (P<0.05) on 10th day and 17th day after operation. CD+4/ CD+8 ratio significantly increased on 17th day after operation (P<0.05). There was no significant difference of the levels of T lymphocyte subsets between the 10th day and 17th day after operation. CONCLUSIONS: The patients with locally advanced lung cancer have a remarkable impairment of immunological function, which mainly show stronger immunosuppression and have some recovery after operation. In the view of immunology, the surgical resection for locally advanced lung cancer shows active significance.     

Retarding effect of simvastatin on artery remodeling induced by high-salt and high-fat diet in rats

AIM: To investigate the effect of simvastatin intervention on the changes of blood pressure, serum lipid fluctuation and aortic configuration induced by high-sodium and high-fat diet in rats. METHODS: Sixty adult male SD rats were randomly divided into 5 groups (n=12): control (N)group, high salt (S)group, high fat (F) group, high salt+ high fat (SF) group and high salt+high fat + simvastatin (T) group. After fed for 16 weeks, the rats were subject to determine blood pressures and serum concentrations of triglycerides (TG),total cholesterol(TC) and soluble CD40 ligand (sCD40L). The expression of CD40/CD40L in the root of ascending aorta was detected by immunohistochemical method. The thickness of intima media in the ascending aorta as well as the ratio of lumen area/total vascular area were measured and calculated after HE staining. RESULTS: In S group, F group and SF group, systolic blood pressure was significantly higher than that in N group (P<0.01). Systolic blood pressure in T group were slightly higher than that in N group with statistical significance and significantly lower than that in SF group. The serum concentrations of TG and TC in F group and SF group were significantly higher than those in N group and T group (P<0.01), and no significant difference among S group, N group and T group was observed. In S group, F group and SF group, the serum concentrations of sCD40L were higher than that in N group and T group (P<0.05), meanwhile that in SF group was also higher than that in S group and F group (P<0.05). However, no significant difference of sCD40L concentration between S group and F group as well as N group and T group was observed. The expression of CD40/CD40L in the ascending aorta in S group, F group and SF group was higher than that in N group and T group (P<0.05), and that in SF group was also higher than that in S group and F group (P<0.05).No significant difference of CD40/CD40L expression between S group and F group as well as N group and T group was observed. The thickness of intima media in S group, F group and SF group was significantly thicker than that in N group (P<0.01), and no significant difference of the intima media thickness between T group and N group was observed. The ratio of lumen area/total vascular area in S group, F group and SF group was smaller than that in N group (P<0.05), and no significant difference of the ratio between T group and N group was found. CONCLUSION: Feeding high-fat and high-salt diet leads to blood pressure elevation, induces atherosclerosis, increases serum concentration of sCD40L and enhances the expression of CD40/CD40L in arterial tissues. The combination of the stimuli has stronger effect than a single factor. Statins protect the arterial tissues against atherosclerosis by decreasing the level of serum sCD40L and inhibiting the arterial expression of CD40/CD40L.     

Effect of prostate-specific membrane antigen on phospho-ERK,growth and migration of prostate cancer LNCaP cells

AIM: To study the expression of prostate-specific membrane antigen (PSMA) on the level of phospho-ERK, cell growth and migration of prostate cancer LNCaP cells.METHODS: The method of silencing PSMA was established by lentivirus-mediated RNAi in our early experiment. The cells were divided into 3 groups.In experimental group, the expression of PSMA in LNCaP cells was stably blocked by lentivirus-mediated RNAi. In negative control group, the cells were transfected with lentivirus-mediated control RNAi (without any interference to PSMA).The normal LNCaP cells served as blank control. The cells in these 3 groups were cultured in both 2 environments: normal medium and medium with PD98059 (an inhibitor of ERK phosphorylation). The phospho-ERK was detected by Western blotting and immunocytochemistry. Furthermore, the growth and migration of the cells were evaluated by MTT and transwell assays,respectively.RESULTS: In normal medium, the expression of phospho-ERK was attenuated in experimental group (P<0.05) and the quantity of "positive" cells was less than those in other 2 groups (P<0.05). Furthermore, the growth curves of the cells showed that the growth ability in experimental group was significantly decreased (P<0.05, after 48 h) and the migration ability in experimental group was reduced (P<0.05). In the inhibitory medium, the cells in all 3 groups expressed phospho-ERK at a lower level. Moreover, the abilities of growth and migration in these 3 groups were poorly displayed. These inhibitory effects on phosphorylation of ERK were similar to the cells in experimental group cultured in normal medium.CONCLUSION: PSMA may play a role in up-regulation of phospho-ERK and it may take an advantage in growth and migration of prostate cancer LNCaP cells.     

Construction of siRNA-survivin and GRIM-19 coexpression plasmid and its growth inhibitory effect on prostatic cancer DU145 cells

AIM: To construct the recombinant plasmid that expresses siRNA-survivin and GRIM-19 simultaneously, and to identify the validity of the recombinant plasmid and observe its effect on expression of survivin and GRIM-19 and proliferation ability of prostate cancer DU145 cells. METHODS: The recombinant plasmid coexpressing siRNA-survivin and GRIM-19 was constructed using gene cloning technique. The prostatic cancer DU145 cells were transfected with the coexpression plasmid and control plasmids. Survivin and GRIM-19 mRNA expression was detected by semi-quantitative RT-PCR. The proliferation ability affected by coexpression plasmid was measured by MTT assay. RESULTS: The coexpression plasmid pGRIM-19-si-survivin was successfully constructed according to DNA recombinant technique and identified through restriction enzyme digestion and plasmid sequencing. Compared with the mock, survivin mRNA expression levels were 0.55?0.05,0.62?0.08 and 0.35?0.05 in psi-survivin, pGRIM-19 and pGRIM-19-si-survivin groups, respectively. Compared with psi-survivin and pGRIM-19, pGRIM-19-si-survivin inhibited survivin mRNA expression markedly (P<0.05), while the expression levels of GRIM-19 mRNA were 1.93?0.14, 2.57?0.20 and 4.12?0.21 in psi-survivin, pGRIM-19 and pGRIM-19-si-survivin groups, respectively (P<0.01). Compared with pGRIM-19 group, pGRIM-19-si-survivin enhanced GRIM-19 mRNA expression more obviously (P<0.05). After transfection for 48 h, the proliferation rates were 58.0%?7.2%, 62.1%?6.1% and 50.2%?4.8% in the 3 experiment groups compared with the mock (P<0.05). After transfection for 72 h, the proliferation rate were 43.4%?4.3%, 51.3%?6.7% and 26.8%?7.1% in experiment groups compared with the mock (P<0.05). Compared with psi-survivin and pGRIM-19, pGRIM-19-si-survivin significantly inhibited the cell growth (P<0.05). CONCLUSION: Transfection of coexpression plasmid pGRIM-19-si-survivin dramatically changes the mRNA expression of survivin and GRIM-19 and inhibits the cell growth.     

Changes of serum prostate specific antigen content,volume of prostate,and serum testosterone content with aging

AIM: To study the relationship between serum prostate specific antigen (PSA) and sex hormones as well as PSA change with aging and volume of prostate. METHODS: Volume of prostate was measured by supersonic diagnostic set. Serum PSA content was determined by ELISA. Serum testosterone and Luteinizxing hormone (LH) contents were measured by radioimmunoassay. The relationship between volume of prostate, PSA , sex hormones and PSA with aging was analyzed. RESULTS: (1) Serum PSA increased with aging. (2) Declined serum levels of testosterone with aging were detected. Serum LH contents increased with aging. (3) PSA and LH contents were positively correlated with aging and volume of prostate. (4) The testosterone levels were negatively correlated with the volume of prostate (r=-0.45,P＜0.01). CONCLUSION: The amount of serum PSA is correlated with the histological changes of the benign hyperplasia of prostate, and the declined serum testosterone is one of the most important reasons of abnormal hyperplasia of prostate.     

Analysis of proteomic spectra in serum from patients with colorectal cancer by SELDI-TOF mass spectrometry

AIM: To study the changes of proteomic spectra in serum from patients with colorectal cancer in order to detect the specific protein markers. METHODS: Proteomic spectra of sixty-four serum samples from patients with colorectal cancer (preoperation and postoperation) and forty from normal individuals were generated by IMAC-Cu proteinchip array and SELDI-TOF mass spectroscopy (surface enhanced laser desorption/ionization-time of flight). The discriminatory profiling between cancer and normal samples was analyzed by Biomarker Wizard software and Biomarker Pattern softwar. RESULTS: Nineteen differentially expressed proteins in serum were screened by analysis of protemic spectra of preoperative patients and normal individuals. Five proteins (5972.67 D, 5927.21 D, 6113.48 D, 5908.55 D and 4292.51 D) were obtained for making up marker patterns that was able to class the patients-team and normal-team. Corresponding correct ratio were 97.5% (56/64) and 80% (32/40). The proteins that overexprssed in preoperation were obviously down-regulated when postoperation. CONCLUSION: The preliminary results suggest that classification system will provide a highly accurate and innovative approach for the early diagnosis of colorectal cancer and judgment of prognosis. SELDI-TOF mass spectrometry is a useful tool for the detection and identification of new protein markers in serum.     

Serum CTRP1 and CTRP7 levels are associated with coronary atherosclerotic heart disease and diabetes mellitus

AIM To investigate the relationship between the serum levels of C1q/TNF-related protein (CTRP) 1 and CTRP7 and coronary atherosclerotic heart disease (CAD) in the patients with or without type 2 diabetes mellitus (T2DM). METHODS Totally 138 cases of participants were selected, and divided into control group (without T2DM or CAD; n=40), T2DM group (with T2DM, but without CAD; n=30), CAD group (with CAD, but without T2DM; n=40), and CAD+T2DM group (with both T2DM and CAD; n=28). The serum levels of CTRP1 and CTRP7 in these participants were measured by ELISA. RESULTS (1) Compared with control group, serum CTRP1 level in CAD group and CAD+T2DM group was significantly increased (P<0.05 or P<0.01), and serum CTRP7 level in CAD, T2DM and CAD+T2DM groups was significantly decreased (P<0.05 or P<0.01). (2) Increased serum CTRP1 level was a risk factor for CAD [odds ratio (OR)=1.136; 95% confidence interval (CI): 1.010~1.278; P=0.034). Sex, hypertension and serum triglyceride level were also correlated with CAD. Decreased serum CTRP7 level was a risk factor for T2DM (OR=0.984; 95% CI: 0.969~0.999; P=0.038). Sex, hypertension and serum high-density lipoprotein cholesterol level were also correlated with T2DM. Increased serum CTRP1 level was a risk factor for CAD+T2DM (OR=1.009; 95% CI: 1.005~1.203; P=0.040). Hypertension was also a risk factor for CAD+T2DM. (3) In CAD group, serum CTRP1 level had certain diagnostic value, and the area under the receiver operating characteristic (ROC) curve (AUC) was 0.670 (95% CI: 0.580~0.760; P=0.001), but serum CTRP7 level had no diagnostic value for CAD. In T2DM group, both serum CTRP1 and CTRP7 levels had diagnostic value, and the AUC values of their ROC curves were 0.607 (95% CI: 0.505~0.710; P=0.032) and 0.665 (95% CI: 0.574~0.756; P=0.001), respectively. In CAD+T2DM group, both serum CTRP1 and CTRP7 levels had diagnostic value, and the AUC values of their ROC curves were 0.666 (95% CI: 0.552~0.781; P=0.007) and 0.632 (95% CI 0.517~0.747; P=0.032), respectively. CONCLUSION Increased serum CTRP1 level and decreased serum CTRP7 level are associated with increased risk of T2DM and CAD. Increased serum CTRP1 level is a risk factor for CAD and CAD+T2DM, while decreased serum CTRP7 level is a risk factor for T2DM. Serum CTRP1 level has certain specificity and sensitivity for the diagnosis of CAD, T2DM and CAD+T2DM, while serum level of CTRP7 has certain specificity and sensitivity for the diagnosis of T2DM and CAD+T2DM.