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.

Docetaxel is a first-line anticancer drug widely used in the treatment of advanced prostate cancer. However, its therapeutic efficacy is limited by its side effects and the development of chemoresistance by the tumor. Using a gene differential expression microarray, we identified 449 genes differentially expressed in docetaxel-resistant DU145 and PC3 cell lines as compared to docetaxel-sensitive controls. Moreover, western blotting and immunohistochemistry revealed altered expression of S100A4, ACKR3 and CDH1in clinical tumor samples. Cytoscape software was used to investigate the relationship between critical proteins and their signaling transduction networks. Functional and pathway enrichment analyses revealed that these signaling pathways were closely related to cellular proliferation, cell adhesion, cell migration and metastasis. In addition, ACKR3 knockout using the crispr/cas9 method andS100A4knockdownusing targeted shRNA exerted additive effects suppressing cancer cell proliferation and migration. This exploratory analysis provides information about potential candidate genes. It also provides new insight into the molecular mechanism underlying docetaxel-resistance in androgen-independent prostate cancer and highlights potential targets to improve therapeutic outcomes.

BackgroundEctopic 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 PreentationA 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.ConclusionRenal 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.

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.

Background Baicalein has exhibited anti-tumor effects against several cells of different origins. However, the potential effects of baicalein on renal cancer has not been investigated. Methods Human A498 and 786-O cell lines were used to investigate the antirenal acitivity of baicalein. CCK-8 assay was used to detect cell viability. Cell migration was assessed by scratch assay and transwell migration assay in vitro. Transwell invasion assay was carried out to evaluate the effect of baicalein on cell invasion. Apoptosis assay was performed to detect cell apoptosis using the Annexin V-FITC/PI apoptosis detection kit. The protein expression of ERK, p-ERK, p38, p-p38, p53, bax, bcl-2 and survivin were measured by WB assay. Results Baicalein significantly inhibited the proliferation of A498 and 786-O cells in a time- and dose-dependent manner. The similar effect of baicalein on cell migration, invasion and cell apoptosis were observed. Mechanismlly, ERK and p38 MAPK pathways account for the anti-tumor effects of baicalein. Conclusions Baicalein can induce apoptosis and inhibit metastasis of renal caner cells through inhibition of the ERK and p38R pathway.