Case report: An ectopic adrenocortical adenoma in the renal sinus.

Background: Ectopic adrenal tissue is rare in adults, with an incidence of only about 1%. We report a rare case of ectopic adrenocortical adenoma in the left renal sinus. Case Preentation: A 57-year-old woman was admitted to the Department of Urology due to "a left kidney tumor" on physical examination. Multislice helical computed tomography (CT) showed the left kidney with an anterior lip mass near the hilum, approximately 2.3 cm × 2.2 cm in size. Preoperative renal artery CT angiography (CTA) showed no obvious abnormality. Laparoscopic resection of the left renal sinus mass was performed, and postoperative pathological findings showed ectopic adrenocortical adenoma. The tumor was a nonfunctional adenoma. Conclusion: Renal ectopic adrenal cortical adenoma is rare. Most of them are nonfunctional adenomas, which cannot be clearly diagnosed by preoperative imaging examination and can often be diagnosed by postoperative pathology.

Effect of Bicalutamide Combined with Docetaxel on Serum PSA and VEGF Levels in Patients with Advanced Prostate Carcinoma.

Objective: To investigate the effect of bicalutamide combined with docetaxel on the levels of prostate-specific antigen (PSA) in serum and vascular endothelial growth factor (VEGF) in patients with advanced prostate carcinoma (PCa). Methods: The clinical data of 103 patients with advanced PCa at our hospital between Feb. 2020 and Feb. 2021 were retrospectively analyzed, the 90 of whom screened by inclusion and exclusion criteria were finally chosen as research objects. They were divided into a control group and an experimental group according to the order of admission, with 45 cases in each group. The control group was treated with conventional treatment, while the experimental group underwent the combination of bicalutamide and docetaxel, and the clinical indices of the two groups were compared. Results: After treatment, the serum indices in the experimental group were remarkably lower than those in the control group (P < 0.001), with remarkably lower incidence of toxic and side effects (P < 0.05) and higher Expanded Prostate Cancer Index Composite (EPIC) scores (P < 0.001) in the experimental group than in the control group. Conclusion: The implementation of bicalutamide combined with docetaxel in patients with advanced PCa is effective in reducing the inflammatory expression and improving quality of life and has a higher safety profile. Compared with conventional treatment, this method is of high application value, and further studies will help establish a better solution for such patients.

Piezoelectric Dynamics of Arterial Pulse for Wearable Continuous Blood Pressure Monitoring.

Piezoelectric arterial pulse wave dynamics are traditionally considered to be similar to those of typical blood pressure waves. However, achieving accurate continuous blood pressure wave monitoring based on arterial pulse waves remains challenging, because the correlation between piezoelectric pulse waves and their related blood pressure waves is unclear. To address this, the correlation between piezoelectric pulse waves and blood pressure waves is first elucidated via theoretical, simulation, and experimental analysis of these dynamics. Based on this correlation, the authors develop a wireless wearable continuous blood pressure monitoring system, with better portability than conventional systems that are based on the pulse wave velocity between multiple sensors. They explore the feasibility of achieving wearable continuous blood pressure monitoring without motion artifacts, using a single piezoelectric sensor. These findings eliminate the controversy over the arterial pulse wave piezoelectric response, and can potentially be used to develop a portable wearable continuous blood pressure monitoring device for the early prevention and daily control of hypertension.

Upregulation of AQP2 mediated by transcription factor FOXO1 inhibits TGF-ß-induced fibrosis in human urothelial cells.

Bladder outlet obstruction (BOO) is a common urological disease, and inhibition of TGF-ß-induced bladder tissue fibrosis may serve as an alternative strategy for BOO treatment. Aquaporin (AQP)2 was reported to be aberrantly expressed in rat BOO, but its specific role was not clarified. The aim of the present study was to explore the role of AQP2 in TGF-ß-induced urothelial cell fibrosis and elucidate the potential underlying mechanism. The SV-HUC-1 human urinary tract epithelial cell line was treated with TGF-ß1 to establish an in vitro model of bladder fibrosis. Cell Counting Kit-8 and wound healing assays were performed to measure cell viability and migration, respectively. Cell transfection was conducted to silence/overexpress AQP2 and Forkhead box O1 (FOXO1). Protein expression was measured using western blotting. Luciferase reporter and chromatin immunoprecipitation assays were used to verify the predicted interaction between AQP2 and FOXO1. The present study found that AQP2 expression was downregulated in TGF-ß1-treated urothelial cells. Overexpression of AQP2 significantly suppressed cell viability, migration and epithelial-to-mesenchymal transition in TGF-ß1-treated SV-HUC-1 cells. In addition, FOXO1 overexpression exerted similar effects as AQP2 overexpression on TGF-ß-treated SV-HUC-1 cells, but these changes were partially abolished by AQP2 knockdown. It was also found that FOXO1 was able to bind to the AQP2 promoter and regulate AQP2 expression. In conclusion, the transcription factor FOXO1 may upregulate AQP2 expression, thereby inhibiting TGF-ß-induced fibrosis in human urothelial cells. The findings of the present study may provide a novel potential strategy for the clinical treatment of BOO by targeting AQP2.

Self-Powered Interactive Fiber Electronics with Visual-Digital Synergies.

Fiber electronics with mechanosensory functionality are highly desirable in healthcare, human-machine interfaces, and robotics. Most efforts are committed to optimize the electronically readable interface of fiber mechanoreceptor, while the user interface based on naked-eye readable output is rarely explored. Here, a scalable fiber electronics that can simultaneously visualize and digitize the mechanical stimulus without external power supply, named self-powered optoelectronic synergistic fiber sensors (SOEFSs), are reported. By coupling of space and surface charge polarization, a new mechanoluminescent (ML)-triboelectric synergistic effect is realized. It contributes to remarkable enhancement of both electrical (by 100%) and optical output (by 30%), as well as novel temporal-spatial resolution mode for motion capturing. Based on entirely new thermoplastic ML material system and spinning process, industrial-level continuously manufacture and recycling processes of SOEFS are realized. Furthermore, SOEFSs' application in human-machine interface, virtual reality, and underwater sensing, rescue, and information interaction is demonstrated.

Hypoxia-induced microRNA-155 overexpression in extracellular vesicles promotes renal cell carcinoma progression by targeting FOXO3.

Renal cell carcinoma (RCC) is a form of cancer arising from the renal epithelium, with high mortality rates that have reached stable levels over the past decade. The tumor microenvironment is an essential regulator of tumor progression and survival, and extracellular vesicles (EVs) are an important facet of this microenvironment. Herein, we explored the impact of hypoxia-induced miR-155 expression in EVs on FOXO3 expression in RCC cells and their associated oncogenic activity. We found that RCC patients exhibited elevated miR-155 expression in EVs relative to healthy controls, suggesting that this miRNA may be important in the context of RCC progression. We then characterized EVs produced from RCC cell lines (Caki-1 and 786-O) under normoxic and hypoxic conditions, revealing that hypoxia-induced EVs contained higher levels of miR-155 and promoted cell proliferation. Then, we identified FOXO3 as a miR-155 target. Lastly, hypoxia-induced EVs were found to be able to significantly inhibit FOXO3 activation via facilitating miR-155 up-regulation. Together, these findings indicate that hypoxia can promote the upregulation of miR-155 in EVs and that this miRNA can act in RCC cells to suppress FOXO3 expression, thereby enhancing cellular tumor progression.

LINC01106 post-transcriptionally regulates ELK3 and HOXD8 to promote bladder cancer progression.

Bladder cancer (BCa) is a kind of common urogenital malignancy worldwide. Emerging evidence indicated that long noncoding RNAs (lncRNAs) play critical roles in the progression of BCa. In this study, we discovered a novel lncRNA LINC01116 whose expression increased with stages in BCa patients and closely related to the survival rate of BCa patients. However, the molecular mechanism dictating the role of LINC01116 in BCa has not been well elucidated so far. In our study, we detected that the expression of LINC01116 was boosted in BCa cells. Moreover, the results of a series of functional assays showed that LINC01116 knockdown suppressed the proliferation, migration, and invasion of BCa cells. Thereafter, GEPIA indicated the closest correlation of LINC01116 with two protein-coding genes, ELK3 and HOXD8. Interestingly, LINC01116 was mainly a cytoplasmic lncRNA in BCa cells, and it could modulate ELK3 and HOXD8 at post-transcriptional level. Mechanically, LINC01116 increased the expression of ELK3 by adsorbing miR-3612, and also stabilized HOXD8 mRNA by binding with DKC1. Rescue experiments further demonstrated that the restraining influence of LINC01116 knockdown on the progression of BCa, was partly rescued by ELK3 promotion, but absolutely reversed by the co-enhancement of ELK3 and HOXD8. More intriguingly, HOXD8 acted as a transcription factor to activate LINC01116 in BCa. In conclusion, HOXD8-enhanced LINC01116 contributes to the progression of BCa via targeting ELK3 and HOXD8, which might provide new targets for treating patients with BCa.

LINC00689 promotes prostate cancer progression via regulating miR-496/CTNNB1 to activate Wnt pathway.

BACKGROUND: Accumulating evidence has proved the significant influence of long non-coding RNAs (lncRNAs) in cancer formation and development, including PCa. METHODS: The role of LINC00689 in PCa was confirmed by RT-qPCR, MTT, colony formation, flow cytometry, western blot and transwell assays. Besides, the binding ability between LINC00689 and miR-496 was validated by using luciferase reporter assay. Then RT-qPCR, RIP and luciferase reporter and western blot assays were employed to verify the interactions among LINC00689, miR-496 and CTNNB1. Furthermore, the rescuing role of CTNNB1 in Wnt pathway was proved by RT-qPCR, TOP/FOP Flash and western blot assays. RESULTS: LINC00689 was upregulated in PCa tissues and cells as well as at the terminal stage. Further, knock down of LINC00689 repressed PCa cell proliferation, migration and invasion, and initiated PCa cell apoptosis. Additionally, miR-496 inhibitor and pcDNA3.1/CTNNB1 could neutralize the prohibitive effects of LINC00689 silencing on cell proliferation, migration and invasion, meanwhile, could offset the encouraging role of knocking down LINC00689 in cell apoptosis. Moreover, CTNNB1 upregulation exerted redemptive function in Wnt pathway inhibited by LINC00689 depletion. CONCLUSIONS: To sum up, LINC00689 promotes PCa progression via regulating miR-496/CTNNB1 to activate Wnt pathway, which may contribute to research about new targets for PCa treatment.

A five-gene signature predicts overall survival of patients with papillary renal cell carcinoma.

BACKGROUND: The present study aims to investigate the gene expression changes in papillary renal cell carcinoma(pRCC) and screen several genes and associated pathways of papillary renal cell carcinoma progression. METHODS: The papillary renal cell carcinoma RNA sequencing (RNA-seq) data set was downloaded from TCGA (The Cancer Genome Atlas). We identified the differentially expressed mRNAs between cancer and normal tissues and performed annotation of differentially expressed mRNAs to figure out the functions and pathways they were enriched in. Then, we constructed a risk score that relied on the 5-mRNA. The optimal value for the patients'classification risk level was identified by ROC analysis. The relationship between mRNA expression and prognosis of papillary renal cell carcinoma was evaluated by univariate Cox regression model. The 5-mRNA based risk score was validated in both complete set and testing set. RESULT: In general, the 5-mRNA (CCNB2, IGF2BP3, KIF18A, PTTG1, and BUB1) were identified and validated, which can predict papillary renal cell carcinoma patient survival. This study revealed the 5-mRNA expression profile and the potential function of a single mRNA as a prognostic target for papillary renal cell carcinoma. CONCLUSION: In addition, these findings may have significant implications for potential treatments options and prognosis for patients with papillary renal cell carcinoma.

Nomograms for predicting long-term overall survival and disease-specific survival of patients with clear cell renal cell carcinoma.

OBJECTIVES: The aim of this study was to establish comprehensive and practical nomograms, based on significant clinicopathological parameters, for predicting the overall survival (OS) and the disease-specific survival (DSS) of patients with clear cell renal cell carcinoma (ccRCC). PATIENTS AND METHODS: The data of 35,151 ccRCC patients, diagnosed between 2004 and 2014, were obtained from the database of the Surveillance, Epidemiology, and End Results (SEER) program. The Kaplan-Meier method and Cox proportional hazards regression model were used to evaluate the prognostic effects of multiple clinicopathological variables on survival. Based on Cox models, a nomogram was constructed to predict the probabilities of OS and DSS for an individual patient. The predictive performance of nomograms was evaluated using the concordance index (C-index) and calibration curves. RESULTS: According to univariate and multivariate analyses, age at diagnosis, sex, race, marital status, surgical approach, tumor node metastasis (TNM) stage, and Fuhrman grade significantly correlated with the survival outcomes. These characteristics were used to establish nomograms. The nomograms showed good accuracy in predicting 3-, 5-, and 10-year OS and DSS, with a C-index of 0.79 (95% CI, 0.79-0.80) for OS and 0.87 (95% CI, 0.86-0.88) for DSS. All calibration curves revealed excellent consistency between predicted and actual survival. CONCLUSION: Nomograms were developed to predict death from ccRCC treated with nephrectomy. These new prognostic tools could aid in improving the predictive accuracy of survival outcomes, thus leading to reasonable individualized treatment.

Detection rate of prostate cancer following biopsy among the northern Han Chinese population: a single-center retrospective study of 1022 cases.

BACKGROUND: Prostate cancer is known to have ethnic and regional differences. The study aimed to clinically evaluate the detection rate of prostate cancer on transrectal ultrasonography (TRUS)-guided prostate biopsy and analyze its characteristics among the northern Han Chinese population at a single center. METHODS: Between October 2009 and September 2016, a total of 1027 Chinese men, who had undergone TRUS-guided prostate biopsy at Qingdao Municipal Hospital, were retrospectively analyzed. Prostate biopsies were performed in the case of an abnormally elevated serum PSA level, and/or abnormal digital rectal examination (DRE) findings, and/or suspicious prostatic imaging findings. RESULTS: Of the 1022 men enrolled in the analysis, 438 patients (42.8%) were diagnosed with prostate adenocarcinoma histologically. When serum PSA levels were divided into five subgroups (less than 4.0, 4.0 to 10.0, 10.0 to 20.0, 20.0 to 100.0, and ≥ 100.0 ng/ml), the detection rates of prostate cancer were 12.4, 15.9, 34.1, 66.2, and 93.8%, respectively. With serum PSA levels of 4.0 to 10.0 ng/ml, the cancer detection rates for a normal DRE and a suspect DRE finding were 13.5 and 58.2%, respectively. Accordingly, the cancer detection rates for a normal imaging and a suspect imaging finding were 13.5 and 58.2%, respectively. Besides, a large proportion of the patients were in the clinically advanced stage. CONCLUSIONS: The present study data reported a relatively higher prostate cancer detection rate of 42.8% and that the majority of the patients presented with clinically advanced prostate cancers within a local clinical urologic practice. An early detection and screening program for prostate cancer is of great need to reduce the burden from this disease among the northern Han Chinese population.

Baicalein inhibits prostate cancer cell growth and metastasis via the caveolin-1/AKT/mTOR pathway.

Prostate cancer (PCa) is lethal type of genitourinary cancer due to its high morbidity and gradual resistance to androgen deprivation therapy. Accumulating evidence has recently suggested that the daily intake of flavonoids is negatively correlated with the risk of cancer. In this study, we aimed to investigate the potential effects of baicalein on androgen-independent PCa cells and the underlying mechanisms through which baicalein exerts its actions. Cell viability and flow cytometric apoptosis assays indicated that baicalein potently suppressed the growth and induced the apoptosis of DU145 and PC-3 cells in a time- and dose-dependent manner. Consistently, the inhibitory effects of baicalein on migration and invasion were also observed in vitro. Mechanistically, we found that baicalein can suppress caveolin-1 and the phosphorylation of AKT and mTOR in a time- and dose-dependent manner. Moreover, the inhibition of the activation of AKT with LY294002 significantly promoted the apoptosis and metastasis induced by baicalein. In conclusion, these findings suggested that baicalein can induce apoptosis and inhibit metastasis of androgen-independent PCa cells through inhibition of the caveolin-1/AKT/mTOR pathway, which implies that baicalein may be a potential therapeutic agent for the treatment of androgen-independent prostate cancer patients.

Somatostatin Derivate (smsDX) Attenuates the TAM-Stimulated Proliferation, Migration and Invasion of Prostate Cancer via NF-κB Regulation.

Tumor development and progression are influenced by macrophages of the surrounding microenvironment. To investigate the influences of an inflammatory tumor microenvironment on the growth and metastasis of prostate cancer, the present study used a co-culture model of prostate cancer (PCa) cells with tumor-associated macrophage (TAM)-conditioned medium (MCM). MCM promoted PCa cell (LNCaP, DU145 and PC-3) growth, and a xenograft model in nude mice consistently demonstrated that MCM could promote tumor growth. MCM also stimulated migration and invasion in vitro. Somatostatin derivate (smsDX) significantly attenuated the TAM-stimulated proliferation, migration and invasion of prostate cancer. Immunohistochemistry revealed that NF-κB was over-expressed in PCa and BPH with chronic inflammatory tissue specimens and was positively correlated with macrophage infiltration. Further investigation into the underlying mechanism revealed that NF-κB played an important role in macrophage infiltration. SmsDX inhibited the paracrine loop between TAM and PCa cells and may represent a potential therapeutic agent for PCa.

Effect of metformin on apoptosis, cell cycle arrest migration and invasion of A498 cells.

Previous studies have demonstrated that metformin (Met) may reduce the risk of cancer development. In the present study, the anti-cancer effects of Met in A498 cells were investigated. It was found that Met inhibited A498 cell proliferation in a time- and dose-dependent manner, as well as induced the activation of AMP-activated protein kinase. It was also demonstrated that Met promoted A498 cell apoptosis and mechanistic studies suggested that this was mediated by the downregulation of B-cell lymphoma 2 and concurrent upregulation of Bcl-2-associated X protein. In addition, it was observed that Met induced G1 cell cycle arrest by decreasing cyclin D1 expression. Furthermore, the results demonstrated that Met reduced A498 cell migration and invasion in vitro by decreasing matrix metalloproteinase-2, which indicated its potential to inhibit renal cancer metastasis. In combination, these results provide evidence that Met is important in anti-renal cancer therapy, and thus may serve as a novel and efficient agent for renal cancer treatment.

Nitidine chloride induces apoptosis and inhibits tumor cell proliferation via suppressing ERK signaling pathway in renal cancer.

Nitidine chloride (NC), a natural bioactive alkaloid derived from Zanthoxylum nitidum (Roxb) DC, has been shown to have inhibitory effects on various tumors. However, whether NC could exert anti-cancer activity and the underlying mechanisms have not been elucidated in renal cancer cells. In this study, we demonstrated the growth inhibitory and pro-apoptotic effects of NC on renal cancer cells both in vitro and in vivo. With cell viability and flow cytometric apoptosis assays, we found that NC potently suppressed the growth of 786-O and A498 cells in a time- and dose- dependent manner. Consistently, the xenograft model performed in nude mice exhibited reduced tumor growth with NC treatment. Mechanically, we presented that NC significantly decreased phosphorylation of ERK and Akt, accompanied by up-regulation of P53, Bax, cleavage caspase-3 and cleavage PARP, downregulation of Bcl-2, caspase-3 and PARP. Furthermore, a specific MEK inhibitor, PD98059, could potentiate the pro-apoptotic effects of NC, which indicated that NC might trigger apoptosis in renal cancer cells partly via inhibition of ERK activity. Taken together, our results imply that NC could be developed as a potential anticancer agent to renal cancer and worthy of further studies.

Nitidine chloride inhibits renal cancer cell metastasis via suppressing AKT signaling pathway.

Nitidine Chloride (NC) has been shown to have anti-cancer effects on various tumors. However, whether NC could exert anti-metastasis activity in renal cancer cells and the underlying mechanisms have not been elucidated. In this work, our data demonstrated the anti-metastasis effects of NC on renal cancer cells in vitro. With scratch assay and transwell assays, we found that NC potently suppressed the migration and invasion of 786-O and A498 cells. Mechanistically, we presented that NC significantly decreased phosphorylation of AKT, accompanied by down-regulation of MMP-2 and MMP-9. Furthermore, a specific AKT inhibitor, LY294002, could enhance the anti-metastasis effects of NC, which indicated that NC suppressed metastasis of renal cancer cells partly via inhibition of AKT activity. Taken together, our results imply that NC can be developed as a potential anti-metastasis agent to renal cancer.

Simvastatin inhibits renal cancer cell growth and metastasis via AKT/mTOR, ERK and JAK2/STAT3 pathway.

Renal cell carcinoma (RCC) is the most lethal type of genitourinary cancer due to its occult onset and resistance to chemotherapy and radiation. Recently, accumulating evidence has suggested stains, inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase, were associated with the risk reduction of cancer. In the present study, we aimed to investigate the potential effects of simvastatin on RCC cells and the underlying mechanisms by which simvastatin exerted its actions. With cell viability, colony formation, and flow cytometric apoptosis assays, we found that simvastatin potently suppressed cell growth of A498 and 786-O cells in a time- and dose- dependent manner. Consistently, the xenograft model performed in nude mice exhibited reduced tumor growth with simvastatin treatment. In addition, the inhibitory effects of simvastatin on migration and invasion were also observed in vitro. Mechanically, we presented that simvastatin could suppress the proliferation and motility of RCC cells via inhibiting the phosphorylation of AKT, mTOR, and ERK in a time- and dose- dependent manner. Further investigation of the underlying mechanism revealed simvastatin could exert the anti-tumor effects by suppressing IL-6-induced phosphorylation of JAK2 and STAT3. In conclusion, these findings suggested that simvastatin-induced apoptosis and its anti-metastasis activity in RCC cells were accompanied by inhibition of AKT/mTOR, ERK, and JAK2/STAT3 pathways, which imply that simvastatin may be a potential therapeutic agent for the treatment of RCC patients.

Somatostatin derivative (smsDX) targets cellular metabolism in prostate cancer cells after androgen deprivation therapy.

Cancer cell metabolism responsive to androgen deprivation therapy (ADT) may be involved in the development and progression of prostate cancer and the ultimate failure of androgen-deprivation therapy. To investigate the metabolism regulation effects on androgen-independent growth of prostate cancer, an established LNCaP-s cell model that resembles the clinical scenario of castration-resistant prostate cancer (CRPC), was used in this current study. This cell line was cultured from androgen-sensitive LNCaP parental cells, in an androgen-reduced condition, resembling clinical androgen deprivation therapy. To assess the effects of smsDX on the invasiveness of prostate cancer cells we used wound healing assay and Matrigel™ invasion assay. We evaluated differentially expressed proteins of the parental LNCaP cells and LNCaP-s cells after ADT by means of two-dimensional gel electrophoresis (2-DE) followed by MALDI-TOF mass spectrometric analysis. The covered area in the wound and the number of cells invading through a Matrigel chamber were significantly smaller for cells treated with smsDX than they were for control cells treated with vehicle. 56 proteins were found differentially expressed in LNCaP-s cells compared to LNCaP cells, majority of them were down-regulated after ADT treatment. 104 proteins of LNCaP cells and 86 in LNCaP-s cells, separately, were found differentially expressed after treatment with smsDX, When we explored these protein functions within the website UniProtKB/Swiss-Prot, surprisingly, most of the proteins were found to be involved in the cellular metabolism and mitochondrial function regulation. LNCaP-s as potential metastatic androgen-independent cancer cells, its metabolism and mitochondrial functions could be altered by a new somatostatin derivative smsDX, the smsDX regulatory effects on metabolism in LNCaP-s deliver more therapeutic information with the treatment of CRPC.

Renal cell carcinoma presenting as exfoliative dermatitis (erythroderma) - a case report.

Many kinds of malignant disorders present as exfoliative dermatitis (erythroderma), however, coincident clearcell renal cell carcinoma (ccRCC) and erythroderma has not been reported. A case of synchronous erythroderma and ccRCC in a 57-year-old man is presented presented here. After the diagnosis of the kidney bulk through CT, the patient had a transperitoneal laparoscopic radical nephrectomy, and the syndrome of the erythroderma disappeared after the surgery. The experience of the current patient suggests that the syndrome of erythroderma may resolve spontaneously after radical nephrotomy.

Induction of G1 cell cycle arrest and apoptosis by berberine in bladder cancer cells.

Bladder cancer is the ninth most common type of cancer, and its surgery is always followed by chemotherapy to prevent recurrence. Berberine is non-toxic to normal cells but has anti-cancer effects in many cancer cell lines. This study was aimed to determine whether berberine inhibits the cell proliferation and induces cell cycle arrest and apoptosis in BIU-87 and T24 bladder cancer cell line. The superficial bladder cancer cell line BIU-87 and invasive T24 bladder cancer cells were treated with different concentrations of berberine. MTT assay was used to determine the effects of berberine on the viability of these cells. The cell cycle arrest was detected through propidium iodide (PI) staining. The induction of apoptosis was determined through Annexin V-conjugated Alexa Fluor 488 (Alexa488) staining. Berberine inhibited the viability of BIU-87 and T24 cells in a dose- and time-dependent manner. It also promoted cell cycle arrest at G0/G1 in a dose-dependent manner and induced apoptosis. We observed that H-Ras and c-fos mRNA and protein expressionswere dose-dependently and time-dependently decreased by berberine treatment. Also, we investigated the cleaved caspase-3 and caspase-9 protein expressions increased in a dose-dependent manner. Berberine inhibits the cell proliferation and induces cell cycle arrest and apoptosis in BIU-87, bladder cancer cell line and T24, invasive bladder cancer cell line. Berberine can inhibit the oncogentic H-Ras and c-fos in T24 cells, and can induce the activation of the caspase-3 and caspase-9 apoptosis. Therefore, berberine has the potential to be a novel chemotherapy drug to treat the bladder cancer by suppressing tumor growth.