Royal jelly (RJ) as a traditional medicinal agent has a variety of pharmacological benefits. In the present study, the effects of the royal jelly were investigated on the urinary bladder cancer cell line 5637 (HTB-9). MTT assay was performed to determine the percent of cell viability at different concentrations of the royal jelly. Moreover, in vitro wound-healing assay was applied to investigate the effects of RJ on cell migration. The activities and gene expression levels of matrix metalloproteinase 2 and 9 were assessed by zymography and Real time PCR, respectively. It was confirmed that royal jelly (RJ) at the concentration of 0. 7 mg/ml exerted a significant inhibitory effect on HTB 5637 CELLS and reduced cell viability to 72% in comparison to the control cultures (P-value<0. 009) during the first 72h of treatment. Furthermore, royal jelly Significantly decreased the bladder cancerous cell migration capacity, and induced a significant decrease in the transcriptional level of the MMP9 after 72h (50% of the controls; Pvalue<0. 049). However, R. J. S did not impose any effect on the expression level and activity of matrix metalloproteinase 2. The results indicated the potential of RJ as a promising natural anti-proliferative and antimetastatic drug.

Background: Bladder cancer is the second common malignancy of genitourinary tract, and transitional cell carcinomas (TCCs) account for 90% of all bladder cancers. Due to acquired resistance of TCC CELLS to a wide range of chemotherapeutic agents, there is always a need for search on new compounds for treatment of these cancers.Coumarins represent a group of natural compounds, which some of them have exerted valuable anti-tumor activities. The current study was designed to evaluate anti-tumor properties and mechanism of action of 7-isopentenyloxycoumarin, a prenyloxycoumarin, on 5637 CELLS (a TCC cell line).Results: MTT results revealed that the cytotoxic effects of 7-isopentenyloxycoumarin on 5637 cancerous CELLS were more prominent in comparison to HDF-1 normal CELLS. This coumarin increased the amount of chromatin condensation and DNA damage in 5637 CELLS by 58 and 33%, respectively. The results also indicated that it can induce apoptosis most probably via activation of caspase-3 in these CELLS. Moreover, propidium iodide staining revealed that 7-isopentenyloxycoumarin induced cell cycle arrest at G2/M stage, after 24 h of treatment.Conclusion: Our results indicated that 7-isopentenyloxycoumarin had selective toxic effects on this bladder cancer cell line and promoted its effects by apoptosis induction and cell cycle arrest. This coumarin can be considered for further studies to reveal its exact mechanism of action and also its anti-cancer effects in vivo.

Introduction: Cancer is considered a significant cause of mortality worldwide, and the mortality rate has been growing significantly in the last decades. The present study aimed to assess the effect of nisin on apoptosis and metastasis of human bladder carcinoma (5637) and renal carcinoma (ACHN) CELLS. Methods: In this experimental study, the 5637 and ACHN cell lines were cultured and treated with diverse densities of nisin. The viability test was evaluated by MTT assay. The gene expression level of BAX, BCL-2, CEA, and Rho-GDI2 was examined by real-time PCR. Results: The 430 and 230μ, g/mL nisin could suppress the proliferation of ACHN and 5637 cell lines, respectively. In both studied cancer CELLS, the expression of BAX, BCL-2, CEA, and Rho-GDI2 genes was significantly augmented with nisin exposure. Conclusions: Our results discovered that nisin has cytotoxic effects on the ACHN and 5637 CELLS and prompts apoptosis over up-regulating the BAX/BCL-2 ratio in the 5637-cell line. Moreover, nisin might suppress the metastasis process via up-regulation of the Rho-GDI2 gene.

Transforming growth factor betas are multifunctional polypeptides in the cytokine superfamily. They have a growth inhibitory role on hemopoietic progenitor CELLS in semisolid colony assay as well as in long-term bone-marrow culture. TGF-ß2 represses stromal CELLS, stem cell factor gene transcription, and decreases the stability of c-kit transcripts in hemopoietic CELLS. TGF- ß also modulates GM-CSF production from human lymphocytes. The present study reveals the TGF- ß2 role in production of GM-CSF in HTB 5637, human bladder carcinoma cell line. HTB 5637 CELLS were treated with 5 ng/mL of human TGF- ß2 viable CELLS were counted and GM-CSF concentrationwas determined. No antiproliferate activity of TGF- ß2 on HTB 5637 cell line was observed. Biological assay showed increased levels of GM-CSF in the supernatant of cultured CELLS. However this increase was lower than that expected from ELISA. Since TGF- ß may be an active suppressor factor regulating hemopoiesis, it seems that some inhibitory factor(s) may be produced (increased) in response to TGF- ß2 treatment.  It has been shown that GM-CSF mRNA content from HTB 5637 cell line is very stable and this stabilization is translational dependent. Using Slot blot and Northern blot analysis, we determined that TGF- ß2 upregulated GM-CSF gene expression in HTB 5637 cell line. The results suggest that TGF- ß2 upregulates the production of GM-CSF gene at the transcriptional level.      

Purpose: This work aims to investigate the effects of Δ Np63 gene down-expression on invasion of bladder carcinoma CELLS in vitro. Materials and Methods: Bladder carcinoma cell lines UM-UC-3 and 5637 were cultured. The expression plasmids encoding Δ Np63 were constructed and transfected into UM-UC-3 and 5637 CELLS. The migration and adhesion of CELLS were detected. The expressions of Δ Np63 and invasion-related zonula occludens protein-1 (ZO-1) in CELLS were determined by real-time polymerase chain reaction (PCR) and western blot analysis. Confocal microscopy was used to observe the location of ZO-1 in CELLS. Results: Results showed that the down-expression of Δ Np63 reduced the migration of UM-UC-3 and 5637 CELLS, decreased the heterogeneity adhesion, and increased homogeneous adhesion. After transfection with Δ Np63, the ZO-1 expression in cell membrane and cell cytoplasm was inhibited, also the ZO-1 mRNA and protein levels in CELLS were significantly decreased. Conclusion: This study indicates thatΔ Np63 gene down-expression can reduce the invasion of bladder carcinoma CELLS in vitro.