Objective: The anti-cancer properties of curcumin, a poliphenol extract from the rhizome of curry, has been confirmed by many investigators. However, low levels of uptake, tissue distribution and rapid metabolism has limited its application as an anti-cancer drug. This study is aimed at increasing curcumin's water solubility due to a biodegradable, neutral and non-toxic micellar nano-carrier called dendrosome. This study intends to evaluate the role of dendrosomal-curcumin (DNC) in bladder cancer cell growth.Methods: We performed the MTT assay, flow cytometry and Annexin V-FLUOS (as an apoptosis detection kit) to evaluate cell death. The genetic mechanism of DNC-induced apoptosis was accomplished by a study of the relative expressions of OCT4A, OCT4B1, SOX-2 and Nanog using real-time PCR.Results: DNC-induced cell death complied with a time and dose-dependent paradigm in the 5637 cell line. Cell cycle analysis revealed that the number of CELLS increased in pre- G1 and gradually decreased in G1 and S phases. This showed the inhibitory property of dendrosomal-curcumin on DNA synthesis. Data from real-time PCR determined that expressions of OCT4A, OCT4B1, SOX-2 and Nanog could be related to 5637 cancer cell growth. Dendrosomal-curcumin significantly suppressed mRNA expression of the above mentioned genes (p<0.01).Conclusion: The data showed that DNC induced apoptosis by suppression of pluripotency genes in 5637 bladder cancer CELLS, which confirmed the useful characteristic of nano-drug in bladder cancer therapy.

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 & aim: Nanotechnology is a new research field with wide applications in cancer management. Among the various metal nanoparticles, silver nanoparticles have been used to treat many cancers due to their high antitumor potential. Despite the potential benefits of these nanoparticles, the extent to which they affect normal CELLS has become a challenge. In addition, their anti-cancer effects on 5637 bladder cancer CELLS have not been well established. The aim of the present study was to determine the anti-cancer effects of silver nanoparticles on the survival of 5637 bladder cancer tumor CELLS in comparison with normal embryonic kidney CELLS HEK-293. Methods: In the present experimental study performed in 2021, the survival of 5637 CELLS of bladder cancer and normal CELLS of embryonic kidney (HEK-293) 24 hours after treatment with 30-50 nm silver nanoparticles with concentrations (0-125). Micrograms per milliliter was evaluated by MTT(dimethyl thiazole-diphenyltetrazolium bromide) test. Morphological changes were also assessed by light microscopy. VEGFA gene expression level and cell migration rate were evaluated by quantitative polymerase chain reaction and scratch testing, respectively. The collected data were analyzed using Shapiro-Wilk statistical tests, one-way and two-way analysis of variance, Tukey post hoc test. Results: The results of the present study indicated that the reduction in survival in 5637 and HEK-293 CELLS after treatment with silver nanoparticles was dose-dependent, which significantly decreased in 5637 tumor CELLS. HEK-293 was more than normal CELLS (p <0. 05). In addition, treatment with concentrations of 50 and 60 μ, g / ml silver nanoparticles significantly reduced VEGFA gene expression (p<0. 05) and inhibited the migration of 5637 bladder cancer CELLS (p<0. 001). Conclusion: AgNPs could reduce the viability of 5637 and HEK-293 CELLS as their inhibitory effects on 5637 CELLS viability were significantly more than HEK-293. Furthermore, AgNPs suppressed the 5637 CELLS migration.

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.