A Novel Insight into Paraptosis-Related Classification and Signature in Lower-Grade Gliomas.

Lower-grade gliomas (LGG) are the most common intracranial malignancies that readily evolve to high-grade gliomas and increase drug resistance. Paraptosis is defined as a nonapoptotic form of programmed cell death, which is gradually focused on patients with gliomas to develop treatment options. However, the specific role of paraptosis in LGG and its correlation is still vague. In this study, we first establish the novel paraptosis-based prognostic model for LGG patients. The relevant data of LGG patients were acquired from The Cancer Genome Atlas database, and we found that LGG patients could be divided into three different clusters based on paraptosis via consensus cluster analysis. Through least absolute shrinkage and selection operator regression analysis and multivariate Cox regression analysis, 10-paraptosis-related gene (PRG) signatures (CDK4, TNK2, DSTYK, CDKN3, CCR4, CASP9, HSPA5, RGR, LPAR1, and PDCD6IP) were identified to separate LGG patients into high- and low-risk subgroups successfully. The Kaplan-Meier analysis and time-dependent receiver-operating characteristic showed that the performances of predicting overall survival (OS) were dramatically high. The parallel results were reappeared and verified by using the Chinese Glioma Genome Atlas and Gene Expression Omnibus databases. Independent prognostic analysis and nomogram construction implied that risk scores could be considered the independent factor to predict OS. Enrichment analysis indicated that immune-related biological processes were generally enriched, and different immune statuses were highly infiltrated in high-risk group. We also confirmed the potential relationship of 10-PRG signatures and drug sensitivity of Food and Drug Administration-approved drugs. In summary, our findings provide a novel knowledge of paraptosis status and crucial direction to further explore the role of PRG signatures in LGG.

Genome-wide CRISPR/Cas9 screening identifies CARHSP1 responsible for radiation resistance in glioblastoma.

Glioblastomas (GBM) is the most common primary malignant brain tumor, and radiotherapy plays a critical role in its therapeutic management. Unfortunately, the development of radioresistance is universal. Here, we identified calcium-regulated heat-stable protein 1 (CARHSP1) as a critical driver for radioresistance utilizing genome-wide CRISPR activation screening. This is a protein with a cold-shock domain (CSD)-containing that is highly similar to cold-shock proteins. CARHSP1 mRNA level was upregulated in irradiation-resistant GBM cells and knockdown of CARHSP1 sensitized GBM cells to radiotherapy. The high expression of CARHSP1 upon radiation might mediate radioresistance by activating the inflammatory signaling pathway. More importantly, patients with high levels of CARHSP1 had poorer survival when treated with radiotherapy. Collectively, our findings suggested that targeting the CARHSP1/TNF-α inflammatory signaling activation induced by radiotherapy might directly affect radioresistance and present an attractive therapeutic target for GBM, particularly for patients with high levels of CARHSP1.

Identification of differentially expressed genes and signaling pathways in human conjunctiva and reproductive tract infected with Chlamydia trachomatis.

BACKGROUND: Currently, Chlamydia trachomatis-specific host defense mechanisms in humans remain poorly defined. To study the characteristics of host cells infected early with Chlamydia trachomatis, we used bioinformatics methods to analyze the RNA transcription profiles of the conjunctiva, fallopian tubes, and endometrium in humans infected with Chlamydia trachomatis. METHOD: The gene expression profiles of GSE20430, GSE20436, GSE26692, and GSE41075 were downloaded from the Gene Expression Synthesis (GEO) database. Then, we obtained the differentially expressed genes (DEGs) through the R 4.0.1 software. STRING was used to construct protein-protein interaction (PPI) networks; then, the Cytoscape 3.7.2 software was used to visualize the PPI and screen hub genes. GraphPad Prism 8.0 software was used to verify the expression of the hub gene. In addition, the gene-miRNA interaction was constructed on the NetworkAnalyst 3.0 platform using the miRTarBase v8.0 database. RESULTS: A total of 600 and 135 DEGs were screened out in the conjunctival infection group and the reproductive tract infection group, respectively. After constructing a PPI network and verifying the hub genes, CSF2, CD40, and CSF3 in the reproductive tract infection group proved to have considerable statistical significance. CONCLUSION: In our research, the key genes in the biological process of reproductive tract infection with Chlamydia trachomatis were clarified through bioinformatics analysis. These hub genes may be further used in clinical treatment and clinical diagnosis.

Remote C6-Enantioselective C-H Functionalization of 2,3-Disubstituted Indoles through the Dual H-Bonds and π-π Interaction Strategy Enabled by CPAs.

A versatile dual H-bonds and π-π interaction strategy that enables enantioselective remote C6-selective C-H functionalization of 2,3-disubstituted indoles was first reported. The N-H bond of indole was pivotal to achieve the C6 functionalization with excellent yield and enantioselectivity. Furthermore, this methodology leads to the efficient construction of numerous enantioenriched C6-functionalized indole products under mild reaction conditions employing different electrophiles. Preliminary cell proliferation investigations revealed that the synthesized chiral C6-substituted indole derivatives had potential anticancer activities.

BACH1 promotes the progression of human colorectal cancer through BACH1/CXCR4 pathway.

The present study was to investigate clinical significance, biological functions and underlying mechanisms of BTB Domain and CNC Homolog 1(BACH1) deregulation in human colorectal cancer (CRC). The result showed that BACH1 upregulation was significantly associated with enhanced tumor invasion (P = 0.014) and gender (P = 0.028) of CRC patients. Kaplan-Meier method results showed that the overall survival of CRC patients with high BACH1 mRNA expression was markedly shorter than those with low expression (P = 0.015), and multivariate analyzes results showed that BACH1 was an independent prognostic predictor for CRC patients (P = 0.049). In vitro studies revealed that BACH1 efficiently promoted invasion and migration of CRC cell line. In vitro studies proved that the HCT116 cell stably expressing BACH1 formed significantly larger tumor nodules and remarkably accelerated tumor xenografts growth. In addition, Immunohistochemical scores of CD31 and Vimentin were significantly higher than those of the control group. Finally, correlation analysis indicated that BACH1 expression was positively correlated with C-X-C Motif Chemokine Receptor 4(CXCR4) in tumor tissues and cell lines. Together, BACH1 serves as an oncogene to promote CRC progression and an independent prognostic factor for survival and metastasis. BACH1 may inhibit the progression of CRC through BACH1/CXCR4 pathway.

Elevated Expression of DLG1 Is Associated with Poor Prognosis in Patients with Colorectal Cancer.

AIMS AND BACKGROUND: Discs large homolog 1 (DLG1) belongs to the modular proteins Membrane Associated Guanylate Kinases (MAGUKs) and plays a major role in the formation of cell-cell junctions and cell polarity. DLG1 varies in expression and localization among malignancies. However, the clinical significance of DLG1 in the context of human colorectal cancer (CRC) remains unclear. The purpose of this study study is to determine the association of DLG1 with clinicopathological characteristics and prognosis of CRC patients. METHODS: DLG1 expression in human CRC was detected by immunohistochemical analysis and validated with mRNA data from a high-throughput sequencing TCGA datasets. The association of DLG1 expression with clinicopathological features in CRC patients was then statistically analyzed. RESULTS: Immunohistochemistry analysis found that DLG1 expression was significantly elevated in CRC tissues, compared with the expression in adjacent non-cancerous colon tissues (P=0.000). High DLG1 expression was significantly associated with advanced clinical stage (P=0.011) and enhanced tumor invasion (P=0.002). The TCGA mRNA expression data revealed that DLG1 mRNA expression was up-regulated in CRC tissues with advanced clinical stage (P=0.008), enhanced tumor invasion (P=0.042), lymph node metastasis (P=0.030), and distant metastasis (P=0.043). Kaplan-Meier survival curves revealed that CRC patients with high DLG1 levels had shorter survival (P=0.040). Furthermore, DLG1 was an independent prognostic factor for CRC patients (HR 2.202, 95% CI 1.057-4.587; P=0.035). CONCLUSIONS: These findings suggest that the increased expression of DLG1 may be predictive of an unfavorable prognosis in CRC patient and serve as a novel therapeutic target in this malignancy.

Case-Control Study on Impact of the Telomerase Reverse Transcriptase Gene Polymorphism and Additional Single Nucleotide Polymorphism (SNP)- SNP Interaction on Non-Small Cell Lung Cancers Risk in Chinese Han Population.

AIMS: To investigate the impact of telomerase reverse transcriptase (TERT) gene polymorphism and additional SNP-SNP interaction on non-small cell lung cancer (NSCLC) risk in Chinese population. METHODS: A total of 828 participants (526 males, 302 females), with a mean age of 71.3 ± 15.7 years old, were selected, including 410 NSCLC patients and 418 normal participants. Logistic regression was performed to investigate association between single nucleotide polymorphism (SNP) and NSCLC risk. Generalized multifactor dimensionality reduction (GMDR) was used to analysis the interaction among four SNPs. RESULTS: Non-small cell lung cancer risk was significantly higher in carriers of G allele of the rs2736100 polymorphism than those with TT (TG + GG vs. TT, adjusted OR (95%CI = 1.68 (1.28-2.07). In addition, we also found that NSCLC risk was also significantly higher in carriers of A allele of the rs2736098 polymorphism than those with GG (GA + AA vs. GG, adjusted OR (95%CI) = 1.52 (1.19-1.93). GMDR analysis indicated that there was a significant two-locus model (P = 0.0100) involving rs2736098 and rs2736100, indicating a potential gene-gene interaction between rs2736098 and rs2736100. Overall, the two-locus models had a cross-validation consistency of 10 of 10, and had the testing accuracy of 62.17%. We found that patients with GA or AA of rs2736098 and TG or GG of rs2736100 genotype have the highest NSCLC risk, compared to patients with GG of rs2736098 and TT of rs2736100 genotype, OR (95%CI) was 2.52 (1.68-3.68), after covariates adjustment. CONCLUSIONS: Minor allele of rs2736098 and rs2736100 in TERT gene and interaction between the two SNP were associated with increased risk of NSCLC risk.

[GLI-1 is involved in EGF-regulated enhancement of the invasiveness of prostate cancer ARCaP(E) cells in vitro].

OBJECTIVE: To investigate the role of the hedgehog (HH) signaling pathway transcription factor glioma-associated oncogene hoinolog 1 (GLI-1) in EGF-regulated enhancement of the invasiveness of the prostate cancer ARCaP(E) cell line in vitro. METHODS: The expressions of EGFR and GLI-1 in prostate cancer ARCaP(E) cells were analyzed by immunofluorescence staining. ARCaP(E) cells were treated with EGF at 100 ng/ml, followed by detection of the changes in cell morphology and invasiveness, as well as in the expressions of p-ERK, ERK and GLI-1. Migration transwell assay was used to determine the effects of 100 ng/ml EGF and GLI-1 antagonist GANT61 on the invasiveness of the ARCaP(E) cells. RESULTS: Both EGFR and GLI-1 were expressed in the ARCaP(E) cells. EGF induced morphological transition of epithelial-like ARCaP(E) cells to mesenchymal-like cells, increased their in vitro invasiveness, and significantly upregulated the expressions of p-ERK and GLI-1 in the ARCaP(E) cells (P<0.05). GANT61 significantly inhibited the in vitro invasiveness of the ARCaP(E) cells and reduced the enhancing effect of EGF on their invasiveness (P<0.05). CONCLUSION: The results from ARCaP(E) cells shed light on the cross-talk of the HH pathway with the EGF/ERK signaling pathway. GLI-1 might be responsible for EGF-regulated enhancement of the invasiveness of ARCaP(E) cells in vitro.

Holmium laser enucleation of the prostate: a modified enucleation technique and initial results.

PURPOSE: Although holmium laser enucleation of the prostate has been proven to be an excellent technique for the treatment of benign prostatic hyperplasia, it has not been widely applied due to technical difficulties and longer operative time. We modified the current technique of enucleation and present our initial experience. MATERIALS AND METHODS: A total of 189 patients with benign prostatic hyperplasia underwent prostatectomy with our modified technique for holmium laser enucleation of the prostate. Intraoperative and postoperative data were prospectively collected. For followup International Prostate Symptom Score, quality of life, maximal flow rate and post-void residual urine were recorded. RESULTS: Mean±SD preoperative prostate volume was 78.1±24.3 cc and 60.9±39.2 gm tissue were enucleated. Mean operative and enucleation times were 54.7±21.1 and 36.5±16.3 minutes, respectively. Mean serum hemoglobin decrease was 0.98±0.72 gm/dl. Mean catheter time was 1.2±0.5 days and mean postoperative hospital stay was 4.9±3.4 days. Serious complications were not observed. Three patients complained of transient stress incontinence which resolved within 3 months. Significant improvement occurred in International Prostate Symptom Score, quality of life, maximal flow rate and post-void residual urine volume at 3 and 6-month followup compared with the preoperative baseline. CONCLUSIONS: The modified holmium laser enucleation of the prostate technique is effective and safe when treating benign prostatic hyperplasia.

[Epithelial-mesenchymal transition and human fetal prostate development].

OBJECTIVE: To investigate the role and significance of epithelial-mesenchymal transition (EMT) and its transcriptional regulator Twist1 in the development of the human fetal prostate. METHODS: Twenty-five human fetal prostate specimens at various developmental stages (16-39 weeks) were included in this study. EMT markers, such as E-Cadherin, N-Cadherin and Vimentin, and EMT transcriptional regulator Twist1 were determined by immunohistochemistry, and their relationship with the development of the human fetal prostate was analyzed. RESULTS: E-Cadherin was expressed in the fetal prostate epithelium only, while Vimentin, N-Cadherin and Twist1 in both the epithelium and the stroma. The expression of E-Cadherin gradually increased, but those of Vimentin, N-Cadherin and Twist1 gradually decreased with the gestation stages. No significant changes were observed in the staining patterns of Vimentin, N-Cadherin and Twist1 in the stroma during the whole developmental process. CONCLUSION: EMT is involved in the development of the human fetal prostate, which may promote epithelial cell motility to form prostatic bud tubules in early gestation stages and boost the differentiation of prostate epithelia in later stages.

[Comparison of transcription factors repressing epithelial phenotype in two different prostate cancer EMT models and its significance].

OBJECTIVE: To screen and compare the specific transcription factors that repress the epithelial phenotype in epithelial-mesenchymal transition (EMT) in two different human prostate cancer models LNCaP/HIF1alpha and ARCaP. METHODS: We established two different prostate cancer EMT models, LNCaP/HIF1alpha and ARCaP, cultured LNCaP, LNCaP/HIF1alpha, IF11 and IA8 cells in vitro, and detected the five transcription factors Snail, Slug, ZEB1, SIP1 and Twist1 in these cells by RT-PCR. RESULTS: Different levels of Snail, Slug, ZEB1, SIP1 and Twist1 were detected in both LNCaP and LNCaP/HIF1alpha cells, with significant differences only in the expressions of Slug and Twist1 between the two cells. The expression of Slug was increased, but that of Twist1 decreased in the LNCaP/HIF1alpha cells. All the five transcription factors but Twist1 were expressed in both the IF11 and IA8 cells, but only the express- sions of ZEB1 and Slug were increased significantly in the IA8 cells. CONCLUSION: There are different mechanisms underlying transcriptional regulation in different prostate cancer EMT models. Slug may be one of the key transcription factors involved in the HIF1alpha-induced EMT of LNCaP cells, while ZEB1 and Slug may play an important role in repressing the epithelial phenotype of the ARCaP model.

[High-dose estrogen inhibits prostate development by down-regulating SHH signaling in new-born SD rats].

OBJECTIVE: To investigate the effects of high-dose estrogen on the development of the prostate in new-born SD rats and its possible relationship with the sonic hedgehog (SHH) signaling pathway. METHODS: One hundred new-born male SD rat pups were assigned to an experimental group, subcutaneously injected with 25 microg Estradiol + 25 microl corn oil vehicle, and a control group, given corn oil alone, on postnatal day (PD) 0, 1, 3 and 5. The animals were sacrificed by decapitation and their prostates removed on PD 1, 6, 10, 20 and 30. The morphological changes of the prostate were observed by HE staining, and SHH signaling related molecules were detected by immunohistochemistry and reverse transcription PCR. RESULTS: High-dose estrogen significantly inhibited the organogenesis of the new-born SD rat prostate and down-regulated the expressions of SHH signaling related molecules. CONCLUSION: High-dose estrogen may restrain the development of the prostate in new-born SD rats via inhibition of SHH signaling.

Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression.

AIM: Silibinin is known to exert growth inhibition and cell death together with cell cycle arrest and apoptosis in human prostate cancer cells. Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate this efficacy and possible mechanisms using a novel highly bone metastatic ARCaP(M) cell model. METHODS: Four prostate cancer cell lines, LNCaP, PC-3, DU145, and ARCaP(M), were used in this study. These cells were treated with increasing concentrations of silibinin (50, 100, and 200 micromol/L) for different periods of time. After treatment, cell viabilities of four prostate cancer cells were compared by MTT assay. Alterations of ARCaP(M) cell invasion, motility and migration were assessed by cell invasion, motility and wound healing assays. The changes of vimentin expression were observed by Western blotting and immunofluorescence staining, and the expression of MMP-2, MMP-9, and uPA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: ARCaP(M) cells showed less sensitivity to the growth inhibition of pharmacological doses of silibinin than LNCaP, PC-3, and DU145 cells. However, silibinin exerted significant dose- and time-dependent inhibitory effects on the invasion, motility and migration of ARCaP(M) cells. Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose- and time-dependent manner after treatment of silibinin. CONCLUSION: This study shows that silibinin could inhibit the invasion, motility and migration of ARCaP(M) cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.

[Transforming growth factor beta upregulates the expression of invasion and metastasis associated proteins in prostate cancer LNCaP cell lines in vitro].

OBJECTIVE: To determine the effect of the transforming growth factor beta (TGF-beta) on the expression of invasion and metastasis associated proteins in the prostate cancer LNCaP cell line in vitro. METHODS: The prostate cancer cell line LNCaP was treated with TGF-beta in vitro. Western blotting was used to detect the expression of the "invasion and metastasis" associated proteins E-Cadherin, N-Cadherin and Vimentin. RESULTS: The expression of N-Cadherin and Vimentin of the LNCaP cells treated with TGF-beta for 12 hours was significantly upregulated, but not that of E-Cadherin. CONCLUSION: TGF-beta may induce epithelial-mesenchymal transition (EMT) of LNCaP cells which might be of importance in promoting prostate cancer cells invading to ambient tissues and metastasizing to distant organs.

Overexpression of coxsackie and adenovirus receptor inhibit growth of human bladder cancer cell in vitro and in vivo.

AIM: To study the effect of the overexpression of coxsackie and the adenovirus receptor (CAR) on the growth of the human bladder cancer cell in vitro and in vivo. METHODS: A retroviral vector pLXSN-CAR expressing CAR was constructed and confirmed by restriction enzyme mapping. The pLXSN-CAR vector and control vector pLXSN were transfected into the PT67 packaging cell line to generate retrovirus with high titer. The CAR-negative T24 cell was infected with the pLXSN-CAR and the pLXSN retrovirus, respectively. The positive clone cells were selected with G418 for 2 weeks. The expression level of the CAR protein was detected by Western blot assay. T24 cell growth in vitro was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Anchorage-independent growth was measured by soft-agar colony formation assay. In vivo cell growth was determined by a nude mice xenograft model. RESULTS: The pLXSN-CAR vector containing full-length CAR cDNA was successfully constructed. Western blot analysis showed that a 46 kDa specific band was found in pLXSN-CA-transfected T24 cells. MTT assay identified the growth inhibition of T24/pLXSN-CAR cells. The cell colony forming ability of T24/pLXSN-CAR cells was significantly lower than that of T24/pLXSN and parental T24 cells. There was a reduction in the tumor size in the T24/pLXSN-CAR group as compared with that of the T24/pLXSN group and parental T24 group. CONCLUSION: The overexpression of CAR in T24 bladder cancer cells can inhibit cell growth both in vitro and in vivo.

[Expression patterns of sonic hedgehog signaling molecules in human fetal prostate development].

OBJECTIVE: To investigate whether the sonic hedgehog signaling pathway is involved in the development of human fetal prostate, and to evaluate the changing staining patterns of its molecules, sonic hedgehog (SHH), patchedl (PTC1), smoothened (SMO), and GLI1, in the human fetal prostate at various gestation stages. METHODS: Fifteen human fetal prostate specimens at various developmental stages (10 - 39 weeks) were included in this study. SHH, PTC1, SMO and GLI1 were detected in all the specimens by immunohistochemical technique. All the slides were observed and assessed under the light microscope. RESULTS: SHH, PTC1, SMO and GLI1 could be detected in human fetal prostate tissues, and their expression formed two surges, the former at week 16, and the latter at week 28. The staining of SHH and SMO was distributed only in the ductal epithelium but not in the stroma. The expression of PTC1 and GLI1 could be found mainly in the epithelium, with minimal staining in the stroma. CONCLUSION: The sonic hedgehog signaling pathway is involved in the development of the human fetal prostate. The high expression of its molecules at early gestation stages might be associated with the induction of prostatic buds, while their abundant expression at later gestation stages might be related to the prostate ductal branching, growth, differentiation and morphogenesis.

[Type IV collagenase expression in human prostate carcinoma cell lines with different metastasis potentials].

OBJECTIVE: To investigate the correlation between type IV collagenase expression and metastatic potential of human prostate carcinoma cells. METHODS: Human prostate carcinoma cell lines (LNCaP and C4-2B) with different metastatic potentials were selected. Using SABC immunocytochemical staining and zymographic analysis, we detected the difference of type IV collagenase expression and activity between the two cell lines. RESULTS: The expression of type IV collagenase (MMP-2, MMP-9) could be detected in both LNCaP and C4-2B, mainly in cytoplasm, much higher in C4-2B than in LNCaP (P < 0.01). The activities of type IV collagenase in the conditioned medium of prostatic carcinoma cell LNCaP was the lowest, and the quantitative estimation values of MMP-2 and MMP-9 were 0.89 +/- 0.02 and 0.86 +/- 0.01, respectively. However, the quantitative estimation values of MMP-2 and MMP-9 in the conditioned medium of C4-2B were 96.32 +/- 4.36 and 33.89 +/- 1.84, respectively. Compared with LNCaP, the activity of type IV collagenase in C4-2B was much higher (P < 0.01). CONCLUSION: Compared with LNCaP, the higher production capability of type IV collagenase in C4-2B may possibly contribute to its invasive and metastatic potentials. The expression of type IV collagenase of human prostate carcinoma cells is closely correlated to the metastatic and invasive potential.

Comparison of seven screening methods in the diagnosis of bladder cancer.

BACKGROUND: We compared the validity (evaluated by sensitivity and specificity), reliability (evaluated by reproducibility) and yield (evaluated by predictive value, examining complexity and cost) of individual and combined tests for bladder tumour antigen stat (BTAstat), nuclear matrix protein 22 (NMP22), hyaluronic acid (HA), survivin, CD44v6, vascular endothelial growth factor (VEGF), and voided urine cytology (VUC) in detecting bladder cancer. And at the same time we evaluated the clinical value of these seven detecting methods in the diagnosis of bladder cancer. METHODS: The six markers and VUC were detected in the urine of cancer group (151 patients with bladder cancer) and two control groups (50 patients with benign urological diseases and 50 healthy controls). The sensitivity, specificity, predictive value, reproducibility, examining complexity and checking cost of each marker and combined markers were calculated. RESULTS: There was a significant difference between bladder cancer group and the two control groups. The sensitivity, specificity and positive predictive value were as follows: VUC (36.4%, 100.0%, 100%), BTAstat (76.8%, 87.0%, 89.9%), NMP22 (77.5%, 81.0%, 86.0%), HA (82.8%, 83.0%, 88.0%), survivin (70.2%, 85.0%, 87.6%), CD44v6 (50.3%, 79.0%, 78.4%), and VEGF (68.2%, 93.0%, 93.6%). The highest sensitivities were 91.4% for NMP22 + BTAstat and HA + NMP22, whereas the combined marker with the lowest sensitivity (62.3%) was VUC + CD44v6. The highest specificity was 93.0% for the combined use of VUC + VEGF and HA + CD44v6 had the lowest specificity (73.0%). The most convenient examining method was the detection for BTAstat, the lowest cost was the detection for HA, and the best reproducibility were the detection for BTAstat and VUC. CONCLUSIONS: All the markers have obvious clinical value in diagnosis of bladder cancer. The use of BTAstat + HA or NMP22 + BTAstat are better examining methods in terms of validity, reliability, and yield.

[Expression and significance of metastasis-associated proteins in prostate cancer cell lines with different metastatic potentials].

OBJECTIVE: To observe the expression profiles between two metastasis-associated proteins in different prostate cancer cell lines and explore the molecular mechanisms of bone metastatic potentials. METHODS: Expressions of E-cadherin and vimentin in two prostate cancer cell lines (LNCaP and IA8) with different metastatic potentials were detected by Western blotting. RESULTS: There was remarkable difference in the expressions of E-cadherin and vimentin between the highly metastatic cell line and the lowly one. As one of the adhesion associated proteins, E-cadherin was detected with high level of expression in LNCaP cell line, which was well known as low metastatic potential. However, E-cadherin did not expressed in IA8 with high metastatic potential. And as one of the cytoskeleton proteins, vimentin expression was high in IA8, but not in LNCaP. CONCLUSION: There is definitely difference in the metastatic phenotypes (E-cadherin and vimentin) among cell lines with different metastatic potentials. The expressions of E-cadherin and vimentin proteins may play important roles in promoting and inhibiting the metastasis of prostate cancer respectively, and may be considered to be valuable in evaluating the malignant degree, predictable metastasis and prognosis of prostate cancers.