Metastasis is the most lethal form of prostate cancer, and finding new therapeutic targets remains a major clinical challenge. TP53 mutation has been identified to be involved in tumor progression and metastasis. Nevertheless, direct evidence of the role of TP53 mutation in prostate cancer metastasis and its underlying mechanism remain obscure. Herein, TP53 was found to be the most mutated gene in prostate cancer, and missense mutations were the primary mutation type based on bioinformatics data analysis. Subsequently, TP53 rs12947788 mutation site was significant in prostate cancer, and correlated with metastasis and tumor-node-metastasis (TNM) stage. Furthermore, forkhead box A1 (FOXA1), a target of TP53, was highly expressed in prostate cancer tissue, especially in TP53-mutant patients. It was also associated with patients' Gleason scores and nodal metastasis. Knockdown of FOXA1 suppressed the migration in prostate cancer cells in vitro. Our findings indicate that targeting TP53 mutation and FOXA1 might be a promising therapeutic target for prostate cancer metastasis.

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.

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.