Mechanisms underlying the formation of main volatile odor sulfur compounds in foods during thermal processing.

Volatile sulfur compounds (VSCs) significantly influence food flavor and garner considerable attention in flavor research due to their low sensory thresholds, diverse odor attributes, and high reactivity. Extensive research studies have explored VSC formation through thermal processes such as the Maillard reaction, thermal pyrolysis, oxidation, and enzymatic reactions. However, understanding of the specific reaction mechanisms and processes remains limited. This is due to the dispersed nature of existing studies, the undefined intermediates involved, and the complexity of the matrices and processing conditions. Given these limitations, the authors have shifted their focus from foods to sulfides. The structure, source, and chemical characteristics of common precursors (sulfur-containing amino acids and derivatives, thiamine, thioglucoside, and lentinic acid) and their corresponding reactive intermediates (hydrogen sulfide, thiol, alkyl sulfide, alkyl sulfenic acid, and thial) are provided, and the degradation mechanisms, reaction rules, and matrix conditions are summarized based on their chemical characteristics. Additionally, the VSC formation processes in several typical foods during processing are elucidated, adhering to these identified rules. This article provides a comprehensive overview of VSCs, from precursors and intermediates to end products, and is crucial for understanding the mechanisms behind VSC formation and managing the flavor qualities of processed foods.

Analysis of parametric instability of cigarettes based on computational fluid dynamics methods.

In actual production tests, there are large fluctuations in the ventilation rate and smoking resistance of cigarettes. In this paper, fluctuations in ventilation rate and smoking resistance are attributed to variations in the number of ventilation holes in the joint paper and the porosity of each component. The effects of small changes in porosity of each component were analyzed by using computational fluid dynamics methods. The results showed that the difference in the effective number of ventilation holes caused by the gluing process had little effect on the ventilation rate and smoking resistance of cigarettes in the practical production process. The smoking resistance is mainly affected by the structural parameters of filter tow and cut tobacco section in the length direction of cigarettes, the porosity of cigarette paper and packaging paper is positively related to the cigarette ventilation rate, the porosity of cut tobacco and the porosity of filter tow are negatively related to the cigarette ventilation rate, and the influence of shaped paper is the smallest. The results can provide technical and theoretical basis for the optimization of cigarette process parameters and the stabilization of ventilation rate.

FAM46B Promotes Apoptosis and Inhibits Glycolysis of Prostate Cancer Through Inhibition of the MYC-LDHA Axis.

OBJECTIVE: Increased dependence on glycolysis is a known element of cancer. This study was designed to examine critical glycolysis components including transcription factor MYC and its downstream target lactate dehydrogenase A (LDHA), potential upstream regulators of glycolysis such as family with sequence similarity 46 member B (FAM46B), and the impact of the abundance of these proteins on apoptosis and glycolysis in prostate cancer. MATERIALS AND METHODS: A total of 70 primary prostate cancer patient samples were compared to normal tissues for FAM46B and LDHA expression and the corresponding patients' survival was monitored for 60 months. Prostate cancer cell lines were employed for protein expression manipulation, glucose uptake and LDH assays, and apoptosis measurements. A xenograft mouse model was used to quantify the role of FAM46B and LDHA on tumor growth in vivo. RESULTS: FAM46B expression was reduced in prostate tumor tissue compared to normal tissue and prostate cancer patients who expressed low amounts of FAM46B had shortened average lifespans compared to those who expressed higher amounts of FAM46B (p=0.008). FAM46B overexpression reduced glucose uptake, decreased LDH activity, and induced apoptosis in prostate cancer cell lines while FAM46B shRNA increased MYC levels in a non-malignant prostate cell line (P69). Conversely, forced expression of LDHA in LNCaP cells produced an increase in glycolysis markers with a corresponding decrease in apoptosis. FAM46B-overexpressing xenografts had starkly blunted growth which was restored with co-overexpression of LDHA. CONCLUSION: FAM46B plays a central role in regulating glycolysis and apoptosis in prostate cancer and operates through the regulation of LDHA via MYC. FAM46B's keystone status in prostate cancer makes it a potential, robust biomarker for prostate cancer prognosis and a promising therapeutic target.

Biosynthesis of selenium nanoparticles and their effect on changes in urinary nanocrystallites in calcium oxalate stone formation.

Plant bio constituents have the ability to prepare nanoparticles, and usually, plant polyphenols are tested to reduce sodium selenite to selenium nanoparticles (SeNPs). In this work, we showed the biosynthesis of SeNPs using Ocimum tenuiflorum leaf extract. The as obtained SeNPs were in the size range of 15-20 nm and spherical in shape. Also, TEM microscopic images represented the aggregation of crystal structures as extracellular deposits. Moreover, scanning electron microscopy was performed to examine the chemical transition of calcium oxalate (CaC2O4) crystal's shape and structure due to the influence of SeNPs. SeNPs inhibited the aggregation and growth of CaC2O4 monohydrate crystals and hence the prepared SeNPs could have important prospects in medical and pharmaceutical applications as a potential inhibitor of CaC2O4 urinary stones.

Down-Regulation of Nfatc1 Suppresses Proliferation, Migration, Invasion, and Warburg Effect in Prostate Cancer Cells.

BACKGROUND Prostate cancer (PCa), accounting for 28% of all male cancer cases, is the second leading cause of cancer-related death among men. NFATc1, belonging to the NFAT family, is overexpressed in PCa and is correlated with the risk of recurrence after radical prostatectomy. MATERIAL AND METHODS In the present study, the expression of NFATc, c-myc, and PKM2 in PCa cells was regulated by lentiviruses and then detected by real-time PCR and Western blot analysis. Further, proliferation, invasion, and migration assays were performed. The glucose consumption and lactate production were assessed by biochemical detection. RESULTS We found that NFATc1 down-regulation significantly suppressed the proliferation and Warburg effect of PCa cells, concurrent with a decrease of c-myc and PKM2 expression. Likewise, the abilities of migration and invasion were also inhibited in NFATc1-silenced PCa cells. In addition, NFATc1 down-regulation-induced inhibition of cell proliferation, migration, invasion, and Warburg effect were counteracted by up-regulation of c-myc or PKM2. The expression of PKM2 was positively regulated by NFATc1 and c-myc expression. CONCLUSIONS These results indicate that NFATc1 down-regulation can suppress the proliferation, Warburg effect, and migration and invasion abilities of PCa cells, probably by regulating c-myc and PKM2 expression. NFATc1 may be a potential therapeutic target for PCa and could be used as a diagnosis or prognosis indicator of PCa.

Hierarchical non-woven fabric NiO/TiO2 film as an efficient anode material for lithium-ion batteries.

Hierarchical non-woven fabric NiO/TiO2 film is prepared using a facile two-step synthesis by electrospinning and subsequent hydrothermal reaction to yield TiO2 film decorated with NiO nanosheets. As an anode material for Li-ion batteries, the NiO/TiO2 composite exhibits discharge and charge capacities of 1251.3 and 1284.3 mA h g-1, with good cycling performance and rate capability. Characterization shows that the NiO nanosheets are distributed on the surface of the TiO2 nanofibers. The total specific capacity of NiO/TiO2 is higher than the sum of pure TiO2 and NiO, indicating a positive synergistic effect of TiO2 and NiO on the improvement of electrochemical performance. The results suggest that non-woven fabric NiO/TiO2 film is a promising anode material for lithium ion batteries.

FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of ß-catenin.

FAM46B is a member of the family with sequence similarity 46. Little is known about the expression and functional role(s) of FAM46B in prostate cancer (PC). In this study, the expression of FAM46B expression in The Cancer Genome Atlas, GSE55945, and an independent hospital database was measured by bioinformatics and real-time PCR analysis. After PC cells were transfected with siRNA or a recombinant vector in the absence or presence of a ß-catenin signaling inhibitor (XAV-939), the expression levels of FAM46B, C-myc, Cyclin D1, and ß-catenin were measured by western blot and real-time PCR. Cell cycle progression and cell proliferation were measured by flow cytometry and the CCK-8 assay. The effects of FAM46B on tumor growth and protein expression in nude mice with PC tumor xenografts were also measured. Our results showed that FAM46B was downregulated but that ß-catenin was upregulated in patients with PC. FAM46B silencing promoted cell proliferation and cell cycle progression in PC, which were abrogated by XAV-939. Moreover, FAM46B overexpression inhibited PC cell cycle progression and cell proliferation in vitro and tumor growth in vivo. FAM46B silencing promoted ß-catenin protein expression through the inhibition of ß-catenin ubiquitination. Our data clearly show that FAM46B inhibits cell proliferation and cell cycle progression in PC through ubiquitination of ß-catenin.

Repair of urethral defects by an adipose mesenchymal stem cell­porous silk fibroin material.

The aim of the present study was to determine whether it was possible to repair urethral defects with a material of adipose mesenchymal stem cells (ADMSCs)­porous silk fibroin (SF). A total of 39 male New Zealand white rabbits were randomly divided into a control group, an SF group and a bromodeoxyuridine (BrdU)­labeled ADMSCs­SF group (SSF group; n=13/group). Defects were made by resecting the posterior urethral wall. The defects in the SF and SSF groups were repaired using SF and BrdU­labeled ADMSCs­SF materials respectively. Then the anterior wall was sutured, and the urethral catheter was retained for 3 weeks following surgery. The catheter was rinsed with nitrofurazone once a day. The cells with positive expressions of factor VIII related antigen (FVIII­RAg), α­smooth muscle actin (α­SMA) and pan­cytokeratin (AE1/AE3) were detected by immunohistochemical assay, and the distributions of BrdU positive cells and macrophages were observed. Urethrography was performed prior to and following surgery. All rabbits had normal urethral morphologies prior to surgery. The incidence rates of postoperative complications in the control, SF and SSF groups were 76.92 (7/13), 23.07 (3/13) and 15.38% (2/13), respectively (P<0.05). The number of positive macrophages in the SSF group was significantly lower than that of the SF group 4 weeks following surgery (P<0.05). In the SSF group, BrdU positive cells were scattered within the SF material following surgery, primarily at the intersection between the SF material and the urethra. The number of FVIII­RAg positive cells in the SSF and SF groups were significantly different (P<0.05), which were also significantly higher than that of control group (P<0.01). The number of α­SMA positive cells in the SSF and SF groups were significantly different (P<0.05), and these values also significantly exceeded those exhibited by the control group (P<0.01). In addition, the SSF and SF groups had positive staining of AE1/AE3. Similar to normal urethral mucosa, the cytoplasm was stained brownish yellow (P<0.05). It is thus feasible to repair urethral defects using ADMSCs­SF material.

Kaempferol Sensitizes Human Ovarian Cancer Cells-OVCAR-3 and SKOV-3 to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-Induced Apoptosis via JNK/ERK-CHOP Pathway and Up-Regulation of Death Receptors 4 and 5.

BACKGROUND Ovarian cancer is the most common gynecological malignancies in women, with high mortality rates worldwide. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor (TNF) superfamily which preferentially induces apoptosis of cancer cells. However, acquired resistance to TRAIL hampers its therapeutic application. Identification of compounds that sensitize cancer cells to TRAIL is vital in combating resistance to TRAIL. The effect of kaempferol, a flavonoid enhancing TRAIL-induced apoptosis in ovarian cancer cells, was investigated in this study. MATERIAL AND METHODS The cytotoxic effects of TRAIL (25 ng/mL) and kaempferol (20-100 µM) on human ovarian cancer cells OVCAR-3 and SKOV-3 were assessed. Effect of kaempferol on the expression patterns of cell survival proteins (Bcl-xL, Bcl-2, survivin, XIAP, c-FLIP) and apoptotic proteins (caspase-3, caspase-8, caspase-9, Bax) were studied. The influence of kaempferol on expression of DR4 and DR5 death receptors on the cell surface and protein and mRNA levels was also analyzed. Apoptosis following silencing of DR5 and CHOP by small interfering RNA (siRNA), and activation of MAP kinases were analyzed as well. RESULTS Kaempferol enhanced apoptosis and drastically up-regulated DR4, DR5, CHOP, JNK, ERK1/2, p38 and apoptotic protein expression with decline in the expression of anti-apoptotic proteins. Further transfection with siRNA specific to CHOP and DR5 indicated the involvement of CHOP in DR5 up-regulation and also the contribution of DR5 in kaempferol-enhanced TRAIL-induced apoptosis. CONCLUSIONS Kaempferol sensitized ovarian cancer cells to TRAIL-induced apoptosis via up-regulation of DR4 and DR5 through ERK/JNK/CHOP pathways.

Curcumin inhibits urothelial tumor development by suppressing IGF2 and IGF2-mediated PI3K/AKT/mTOR signaling pathway.

We have previously reported that curcumin inhibits urothelial tumor development in a rat bladder carcinogenesis model. In this study, we report that curcumin inhibits urothelial tumor development by suppressing IGF2 and IGF2-mediated PI3K/AKT/mTOR signaling pathway. Curcumin inhibits IGF2 expression at the transcriptional level and decreases the phosphorylation levels of IGF1R and IRS-1 in bladder cancer cells and N-methyl-N-nitrosourea (MNU)-induced urothelial tumor tissue. Ectopic expression of IGF2 and IGF1R, but not IGF1, in bladder cancer cells restored this process, suggesting that IGF2 is a target of curcumin. Moreover, introduction of constitutively active AKT1 abolished the inhibitory effect of curcumin on cell proliferation, migration, and restored the phosphorylation levels of 4E-BP1 and S6K1, suggesting that curcumin functions via suppressing IGF2-mediated AKT/mTOR signaling pathway. In summary, our results reveal that suppressing IGF2 and IGF2-mediated PI3K/AKT/mTOR signaling pathway is one of the mechanisms of action of curcumin. Our findings suggest a new therapeutic strategy against human bladder cancer caused by aberrant activation of IGF2, which are useful for translational application of curcumin.

MicroRNA-21 Regulates the Proliferation, Differentiation, and Apoptosis of Human Renal Cell Carcinoma Cells by the mTOR-STAT3 Signaling Pathway.

MicroRNA-21 (miRNA-21), a kind of short, noncoding RNAs, functioned as a tumor marker and was upregulated in renal cell carcinoma (RCC). However, the underlying mechanisms of miRNA-21 in RCC were uncertain. Therefore, the effects and mechanisms of miRNA-21 on the proliferation, differentiation, and apoptosis of cultured human RCC cells were further investigated in this study. After slicing miRNA-21 in RCC cells, the viability, mRNA expression of C/EBPα and PPARγ, caspase 3 activity, and protein expression of mTOR, STAT3, and pSTAT3 were determined. It was found that knockdown of miRNA-21 downregulated the optical density (OD) value of cells, inhibited mRNA expression of PPARγ and C/EBPα, and enhanced activity of caspase 3. Furthermore, protein expression of pSTAT3 was also decreased in the absence of miRNA-21. Notably, miRNA-21-changed proliferation, differentiation, and apoptosis of human RCC cells were partially regulated following the block of the mTOR-STAT3 signaling pathway by the mTOR inhibitor (XL388). It was indicated that miRNA-21 promoted proliferation and differentiation and decreased apoptosis of human RCC cells through the activation of the mTOR-STAT3 signaling pathway.

[Spatial distribution of sulfur dioxide around a tobacco bulk-curing workshop cluster].

In order to manifest lower energy consumption and less labor employment, and provide the theoretical basis for constructing environmentally friendly modem tobacco agriculture, this paper analyzed gas composition of the chimney from a bulk-curing barn and the dispersion of sulfur dioxide (SO2) around the workshop cluster using ecom-J2KN flue gas analyzer and air sampler. During curing, the concentrations of carbon dioxide (CO2) and SO2 in the chimney were both highest at 38 degrees C, while the concentration of nitrogen oxides (NOx) was highest at 42 degrees C. The emission concentration of SO2 from the chimney was 1327.60-2218.40 mg x m(-3). Average SO2 emission would decrease by 49.7% through adding 4.0% of a sulfur-fixed agent. The highest concentrations of SO2 in the surface soil appeared at the yellowing stage. SO2 concentration in horizontal direction localized at 43-80 m exceeded 0.5 mg x m(-3). The highest concentration of SO2 (0.57 mg x m(-3)) was observed at 50 m. At 50 m in the downstream wind direction of the workshop cluster, SO2 concentration in vertical direction localized at 0.9-1.8 m exceeded 0.5 mg x m(-3), and the highest concentration of SO2 in vertical direction was 0.65 mg x m(-3) at 1.6 m. During curing, the average concentration of SO2 was decreased by 0.43 mg x m(-3) by using the sulfur-fixed agent. The polluted boundary was localized at 120 m in the downstream wind direction of the workshop cluster.

Fisetin, a dietary flavonoid, induces cell cycle arrest and apoptosis through activation of p53 and inhibition of NF-kappa B pathways in bladder cancer cells.

There is an obvious urgent need to find effective and safe therapies to prevent both recurrence and progression of bladder cancer. In the present study, we report that fisetin-induced apoptosis in human bladder cancer is mediated via modulation of two related pathways: up-regulation of p53 and down-regulation of NF-kappa B activity, causing a change in the ratio of pro- and anti-apoptotic proteins. The results showed that fisetin inhibited the proliferation of T24 and EJ cells by inducing apoptosis and blocking cell cycle progression in the G0/G1 phase. Western blot assay showed that fisetin significantly increases the expression of p53 and p21 proteins, and decreases the levels of cyclin D1, cyclin A, CDK4 and CDK2, thereby contributing to cell cycle arrest. In addition, fisetin increased the expression of Bax and Bak but decreased the levels of Bcl-2 and Bcl-xL and subsequently triggered mitochondrial apoptotic pathway. Our study suggests that the activation of p53 and inhibition of the NF-kappa B system may play important roles in the fisetin-induced apoptosis in bladder cancer cells.

Dendritic cell transfected with secondary lymphoid-tissue chemokine and/or interleukin-2 gene-enhanced cytotoxicity of T-lymphocyte in human bladder tumor cell S in vitro.

OBJECTIVES: The aim of this study was to investigate whether dendritic cells (DCs) transfected with human secondary lymphoid-tissue chemokine (hSLC) and human interleukin-2 (hIL-2) genes are capable of improving DC's proliferation and to produce a marked antitumor effect in vitro combined with T-lymphocyte (TC). METHODS: SLC gene primer was designed based on the corresponding gene sequence in GenBank. The Kpn I site was introduced into the upstream of the primer and Xho I site into the downstream. The SLC gene was amplified with the template of pET32a(+)-SLC by polymerase chain reaction. SLC was cloned into pBudCE4.1/IL-2 (TRAIL was cut from pBudCE4.1/TRAIL- IL-2 before) to construct recombinant plasmid pBudCE4.1/SLC-IL-2(PSI). DCs were transfected with pBudCE4.1/SLC-IL-2 by gene electric transfection. Protein expression was determined with Western blot and enzyme-linked immunosorbent assays. Cytotoxicity of TC and DC against the human bladder tumor cell were examined by chromium release assay. Flow cytometric analyses were performed to determine the apoptosis of tumor cells and the percentage of Treg. RESULTS: A high level of expression of SLC and IL-2 was observed in DCs transfected with SLC and IL-2 genes. The mean production of IL-2 was 19.8 +/- 2.5, 511.10 +/- 52.36, and 541.3 +/- 62.04 ng/10(6) cells/24 hours in the DC/vector, DC/IL-2, and DC/SLC-IL-2, respectively. The mean SLC production was 29.8 +/- 4.43, 506.10 +/- 42.36, and 567.34 +/- 52.05 ngs/10(6)cells/24 hours in the DC/ vector, DC/SLC, and DC/SLC-IL-2, respectively. Cytotoxicity to bladder cancer cells was increased. The mean cytotoxicity (the effector/target ratio, 40:1) of TC-DC/parental, TC-DC/IL-2, TC-DC/SLC, and TC-DC/SLC-IL-2(TDSI) to the human bladder cancer cells was 32.1 +/- 5.5%, 63.5 +/- 6.6%, 78.1 +/- 9.63%, respectively. The apoptotsis rate of bladder cancer cells treated with TDSI was 18.6% by flow cytometry. Treg cells' percentage was very small in the DC medium. CONCLUSIONS: SLC and IL-2 were produced by autocrine in DCs transfected with SLC and IL-2 genes. DC/SLC-IL-2 can promote DC proliferation, while TC-DC/SLC-IL-2 and TC-DC/SLC could strongly enhance significant cytotoxicity against bladder cancer cell that was induced by the coculture of DCs (transfected with SLC and IL-2) and TC.

Two hour exposure to sodium butyrate sensitizes bladder cancer to anticancer drugs.

OBJECTIVES: To investigate the inhibitory effect of sodium butyrate (NaB) on the proliferation of human bladder cancer cell lines and its synergetic effect with anticancer drugs in treating bladder cancer in vitro and in vivo. METHODS: The inhibitory effects of NaB on human bladder cancer cell lines in vitro and the synergetic effect of NaB with mitomycin c, cisplatin (CDDP) and adriamycin were detected by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. Hoechst staining and electron microscopy were used to observe morphology for apoptotic cells after NaB treatment. Fas, bcl-2 and caspase-3 were determined with flow cytometry. In vivo synergetic effects were detected in N-methyl-N-nitrosourea induced bladder cancer model rats. RESULTS: NaB significantly inhibited the growth of bladder cancer cell lines in a concentration and time dependent manner. Better results of tumor inhibition have been achieved when NaB was combined with CDDP, mitomycin c and adriamycin, rather than used alone. Furthermore, 2 h exposure to NaB can sensitize bladder cancer to chemotherapy agents. The Bcl-2 expression in bladder cancer cells is decreased and caspase-3 expression increased after NaB treatment. Intravesical application of NaB combined with CDDP can significantly inhibit tumor growth and progression. CONCLUSIONS: NaB has a direct anticancer effect and can markedly enhance the action of several chemotherapy agents. 2 h expose to NaB can also sensitize bladder cancer to anticancer drugs. NaB may be an excellent candidate agent for intravesical application in treating bladder cancer.

Effects of curcumin on bladder cancer cells and development of urothelial tumors in a rat bladder carcinogenesis model.

Curcumin, a well-known dietary pigment derived from Curcuma longa, inhibited growth of several types of malignant cells both in vivo and in vitro. Its effects on cell proliferation and the induction of apoptosis in human bladder cancer cell lines and intravesical activity in a rat bladder tumor model were studied. Exposure of human bladder cancer cells to curcumin resulted in the induction of apoptotic cell death and caused cells to arrest in the G2/M phase. The anti-apoptotic Bcl-2 and Survivin protein was downregulated by the curcumin treatment together with enhancement of the Bax and p53 expression. The inhibitory activities of curcumin were stronger than those of cisplatin and could not be prevented by catalase pretreatment in T24 cells. Clonal assay indicated large-dose and short-term curcumin was lethal to bladder cancer cells. Moreover, the in vivo study revealed curcumin did induce apoptosis in situ, inhibit and slow the development of bladder cancer. These observations suggest that curcumin could prove an effective chemopreventive and chemotherapy agent for bladder cancer.

Interactions between Oat beta-Glucan and calcofluor characterized by spectroscopic method.

This paper describes the binding of Calcofluor, a fluorescent probe, to oat beta-glucan in buffer solutions. The binding equilibrium constant (K), the total number of binding sites per beta-glucan molecule (N), and the average binding number of Calcofluor per beta-glucan molecule (n) were determined by UV spectroscopic method. The results indicate that the association of Calcofluor and beta-glucan is driven by both enthalpy and entropy and that the process involves hydrogen bonding, van der Waals forces, and hydrophobic interaction. Higher buffer concentration and NaCl facilitate the binding of Calcofluor to beta-glucan. The adsorption isotherm fits a Langmuir model quite well.

Growth inhibitory effects of quercetin on bladder cancer cell.

Quercetin, a flavonoid found in many fruits and vegetables, belongs to an extensive class of polyphenolic compounds. Previous studies reported that quercetin inhibits the proliferation of various cancer cells and tumor growth in animal models. We investigated the growth inhibition and colony formation of quercetin on three bladder cancer cells (EJ, J82 and T24). The expression of tumor suppressor genes and oncogenes such as P53, Survivin, PTEN, as well as the methylation status of these genes was also evaluated. We observed that quercetin induced apoptosis in bladder cancer cells in a time- and dose-dependent manner. Quercetin (100 micromolars) significantly inhibited EJ, T24 and J82 cell growth accompanied by an increase in the G0/G1 phase. In all cell lines, quercetin decreased the expression of mutant P53 and Survivin proteins. However, there was no change in the level of PTEN protein. Moreover, the DNA methylation levels of the estrogen receptor (Er-beta), P16INK4a and RASSF1A were strongly decreased (from 35 to 70%) in the quercetin-treated group compared to the control. In conclusion, our study suggested that quercetin inhibits growth, colony formation and hypermethylation of bladder cancer cell lines. Quercetin-induced apoptosis might be associated with a decrease in mutant P53 and Survivin proteins.