Association between 5α-reductase inhibitors therapy and incidence, cancer-specific mortality, and progression of prostate cancer: evidence from a meta-analysis.

5α-reductase inhibitors (5-ARI) are widely employed for the treatment of benign prostatic hyperplasia. It has been noted that 5-ARI exhibit the potential to attenuate the risk of prostate cancer, but consistent agreement has not been achieved. Moreover, the effect of 5-ARI on cancer-specific mortality and progression of prostate cancer remains unclear. Therefore, the goal of the current meta-analysis was to elucidate the impact of 5-ARI on the incidence and progression of prostate cancer. We searched for all studies assessing the effect of 5-ARI on risk of prostate cancer in PubMed, Embase, Medline, and Cochrane Library databases. Pooled relative risk (RR) and corresponding 95% confidence intervals (CIs) were accepted to evaluate the association between 5-ARI and the risk of prostate cancer. Synthetic results implied that subjects who accepted 5-ARI compared with the placebo group experienced a distinctly weakened overall incidence of prostate cancer (RR = 0.74; 95% CI: 0.66-0.82; P < 0.001). Subgroup analyses further revealed that 5-ARI reduction of the incidence of prostate cancer was limited to low-grade (Gleason score 2-6; RR = 0.68; 95% CI: 0.57-0.81; P < 0.001) and intermediate-grade tumors (Gleason score 7; RR = 0.81; 95% CI: 0.67-0.97; P = 0.023), but not high-grade tumors (Gleason score >7; RR = 1.19; 95% CI: 0.98-1.43; P = 0.069). The results also showed that 5-ARI treatment did not significantly alter prostate cancer-specific mortality (RR = 1.0; 95% CI: 0.95-1.05; P = 0.916). In addition, it was worth noting that 5-ARI treatment acted in a protective role that presented a dramatic benefit to delay the progression of low-risk tumors (RR = 0.58; 95% CI: 0.43-0.78; P < 0.001).

Effect and Mechanism of EGFL7 Downregulation in Human Osteosarcoma Cells on the Biological Function of Co-cultured HUVEC.

BACKGROUND: Even though epidermal growth factor-like domain 7 is known to be overexpressed in osteosarcoma and is associated with poor clinical outcome, few reports are available regarding its mechanism. AIMS: The objective of this study was to explore the effect and mechanism of downregulating epidermal growth factor-like domain 7 expression in a human osteosarcoma cell line on the biological function of co-cultured human umbilical vein endothelial cells. STUDY DESIGN: Cell study. METHODS: In the present study, human osteosarcoma cell lines U2OS, Saos-2, HOS, and MG63, and normal human osteoblasts were cultured in Dulbecco's Modified Eagle Medium containing 10% fetal bovine serum and 1x antibiotics at 37 °C and 5% CO2 in an incubator. Of the four osteosarcoma cell lines, U2OS expresses the highest level of epidermal growth factor-like domain 7 mRNA as determined using quantitative reverse transcription polymerase chain reaction. With the knockdown of epidermal growth factor-like domain 7 in U2OS and human umbilical vein endothelial cells by lentivirus, the proliferation and apoptosis of U2OS and human umbilical vein endothelial cells were investigated using MTT and flow cytometry assays. After the co-culture of human umbilical vein endothelial cells and epidermal growth factor-like domain 7-knockdown U2OS, the in vitro effects on cell proliferation, apoptosis, adhesion, migration, and the angiogenic ability of human umbilical vein endothelial cells were detected using MTT, flow cytometry, Transwell, and tube formation assays, respectively. The expressions of phosphoinositide 3-kinase, phospho-Akt, total Akt, and vascular endothelial growth factor in human umbilical vein endothelial cells were detected using western blot assay. RESULTS: Lentivirus with epidermal growth factor-like domain 7 shRNA could not significantly affect the proliferation and apoptosis of both U2OS and human umbilical vein endothelial cells, whereas the knockdown of epidermal growth factor-like domain 7 in U2OS could significantly inhibit the migration, adhesion, and angiogenic ability of co-cultured human umbilical vein endothelial cells. In addition, the expressions of phosphoinositide 3-kinase, phospho-Akt, and vascular endothelial growth factor in human umbilical vein endothelial cells decreased after co-culturing with epidermal growth factor-like domain 7-knockdown U2OS. CONCLUSION: Epidermal growth factor-like domain 7-knockdown U2OS cells inhibit the migration, adhesion, and angiogenesis of co-cultured human umbilical vein endothelial cells by diminishing phosphoinositide 3-kinase, Akt signaling pathway activity and vascular endothelial growth factor expression.

Decreased expression of microRNA-130a correlates with TNF-α in the development of osteoarthritis.

OBJECTIVE: Increased expression of tumor necrosis factor a (TNF-α) has emerged as an important inflammatory factor in osteoarthritis (OA) and other joint diseases. The study was performed to investigate whether the expression of TNF-α in human chondrocytes was regulated by miRNAs. METHODS: MiRNA-130a and TNF-α expression in cartilage specimens was examined in patients with knee osteoarthritis, chondrocytes and osteoarthritis rat model. Chondrocytes were transfected with siRNAs as a gene silencing methods. Expression of genes and proteins were analyzed by real-time PCR and western blotting respectively. RESULTS: Increased TNF-α and decreased miRNA-130a were observed in tissues from osteoarthritis patients. Moreover, we found a highly negitive correlation between miRNA-130a and TNF-α. Next, miRNA-130a loss-of-function increased the expression of TNF-α and promoted inflammation in chondrocytes. It was reasonable that miRNA-130a regulated a distinct underlying molecular and pathogenic mechanism of OA by forming a negative feedback loop with TNF-α. Furthermore, there were the abnormalities of bone metabolism in OA rat, which showed the miRNA-130a and TNF-α dysfunction that was one of important factors for the occurrence and development of OA. CONCLUSIONS: Our results indicated that miR-130a played an important role in regulating the expression of TNF-α in human chondrocytes and identified miR-130a as a novel therapeutic target in OA.

Perforated sarcomatoid carcinoma of the jejunum: Case report.

Sarcomatoid carcinomas exhibit features that are common to epithelial and mesenchymal tumors. These carcinomas are rare, particularly in the small intestine. In the current case report, we describe a case of an intestinal sarcomatoid carcinoma in a 70-year-old Chinese female. Sarcomatoid carcinoma was confirmed based on light microscopy and immunohistochemical observations. The patient presented with symptoms of acute abdomen, which was due to an intestinal perforation caused by sarcomatoid carcinoma of the small bowel. Patients with sarcomatoid carcinoma are usually associated with a poor prognosis. However, this patient experienced a relatively favorable prognosis, which may be attributed to low positivity for Ki67 in the tumor.

[Effect of C(1-2) venous sinus upon operative safety of atlantoaxial screw insertion].

OBJECTIVE: To introduce a new C(1) screw insertion technique to avoid injury to C(1-2) venous sinus in posterior atlantoaxial fixation. METHODS: 48 cases (96 sides of C(1) screws) undergoing posterior atlantoaxial fixation were retrospectively analyzed, including 28 cases of C(1) or C(2) fresh fracture and 20 cases of congenital malformation or old fracture & dislocation, among which 12 cases (24 sides) were operated by Goel lateral mass screws, 14 cases (28 sides) by TAN Mingsheng C(1) transpedicular screws and 44 sides of C(1) screws in 22 cases were inserted via notch on underside of C(1) posterior arch combined with bone wax column protecting C(1-2) venous sinus. RESULTS: Bleeding was encountered in five sides of C(1) screws among 26 cases (52 sides) whose venous sinuses were not protected by bone wax column, involving 3 cases of Goel lateral screw implant fixation. There was statistical difference in the incidence rate of bleeding between Goel technique and ours (P < 0.05) while there was no statistical difference between C(1) transpedicular technique and ours (P > 0.05) or between Goel sides of Goel lateral mass screws (12.5%) and 2 sides of C(1) transpedicular screws (7.1%). It occurred in none of 22 cases (44 sides) with our presented technique. There was a significant difference between Goel lateral screw implant fixation and C(1) transpedicular technique (P > 0.05). All the screws were implanted successfully. All cases were followed up and there was not any sign of implant failure. CONCLUSIONS: Our presented C(1) screw insertion technique can provide a better bony landmark and vascular protection, stronger bony holding power and more extensive applicability to reduce injury to C(1-2) venous sinus and increase the surgical safety.

[Experimental research of the inhibition of vascular endothelial growth factor C expression in gastric cancer by targeting RNA interference].

OBJECTIVE: To construct the plasmid expression vector pSIH1-H1-copGFP for RNA interference against vascular endothelial growth factor C (VEGF-C) and to evaluate its effect on the expression of VEGF-C mRNA in gastric cancer cells after transfection. METHODS: Three siRNAs of genome sequence of VEGF-C gene were retrieved from GenBank and one negative chain was used as control. Four siRNAs were cloned into plasmid pSIH1-H1-copGFP,which were then transfected into gastric cancer cells (SGC7901). The expression of VEGF-C mRNA was analyzed by RT-PCR. RESULTS: The recombinant plasmid of pSIH1-H1-copGFP specific for VEGF-C was confirmed by gene sequencing analysis. The target sequence obtained was completely consistent with the design. Transfection efficiency of the three siRNAs ranged from 60% to 70%. After transfection, the expression of VEGF-C mRNA in SGC7901 cells was significantly inhibited. Inhibition rates of VEGF-C mRNA expression were 35.4%, 33.8% and 81.5% in the three siRNA plasmid vectors, respectively. CONCLUSION: The siRNA expression plasmid vector against VEGF-C mRNA is successfully constructed, and RNAi may be a useful technique to inhibit the lymphangiogenesis of gastric cancer.