Network pharmacology analysis of Icariside II against bladder cancer.

As a global health threat, bladder cancer (BC) is a common urological disease characterized by a high risk of progression and recurrence. Icariside II (ICA-II), a flavonol glycoside, exhibits antitumor ability in various tumors. However, there is no systematic study exploring the pharmacological mechanism of ICA-II in BC. We used public databases to obtain potential targets of ICA-II and related genes in BC. Bioinformatics analysis and molecular docking were used to identify potential targets and signaling pathways. Then, MTT, cell cycle assays and western blot (WB) were used to validate the predicted pathways in bladder cell lines, and in situ bladder cancer models were also established to verify the effect of ICA-II. Our research demonstrated that these ICA-II hub genes were related to the cell cycle. Then, our molecular docking analysis confirmed the interaction between ICA-II and CCNB1. In addition, our in vitro experiment demonstrated that ICA-II restrained the proliferation of BC cells mainly by blocking the cell cycle. WB also verified that ICA-II decreased the expression levels of CCNB1. In situ BC models showed that ICA-II had no hepatotoxicity or nephrotoxicity and could suppress the growth of in situ BC. In summary, during this study, we found that ICA-II had low toxicity in the kidney and liver. Network pharmacology was used, and both cell and animal experiments verified that ICA-II has a good therapeutic effect on bladder cancer, which may inhibit the proliferation and progression of bladder cancer by blocking the cell cycle of BC cells.

Analysis of Risk Factors for Early Progression of Prostate Cancer After Initial Endocrine Therapy.

Background: Prolonged androgen deprivation therapy (ADT) in patients with prostate cancer can eventually lead to the development of castration-resistant prostate cancer (CRPC). Once CRPC occurs, the patient's prognosis will be inferior. However, the risk factors for progression to CRPC in a short period of time are unclear. Methods: We retrospectively analyzed prostate cancer patients who received their first ADT between January 1, 2015 and January 1, 2021. The main statistical methods used were a logistic regression model and Kaplan-Meier survival analysis. Results: Among 159 prostate cancer patients initially treated with ADT, 90 were screened for inclusion. Patients who progressed to CRPC after ADT were included in group B and others were included in group A. Group B was divided into group B1 and B2 according to whether CRPC progressed within 18 months. Multi-factor logistic regression analysis showed that the time to PSA nadir (TTN) (p = 0.031) and serum lactate dehydrogenase (LDH) (p = 0.013) were significantly different between Group A and B. TTN (p < 0.001), LDH (p = 0.001) and platelet to lymphocyte ratio (PLR) (p = 0.005) were significantly different between Group B1 and B2. Kaplan-Meier survival analysis and log-rank tests showed that TTN, LDH, and PLR statistically differed in CRPC patients' progression-free survival. The ROC curve showed the AUC value of TTN combined with PLR and LDH increased to 0.958 (95% CI 0.911-0.997, p < 0.001). The Chi-square test showed that the expression of p63 in group A was higher than that in groups B1 (p = 0.002) and B2 (p = 0.001). Conclusion: Lower TTN, higher LDH and PLR were associated with early CRPC occurrence after ADT in hormone-sensitive prostate cancer patients. p63 expression was associated with favorable prognosis in prostate cancer patients.

The effect of SSRIs on Semen quality: A systematic review and meta-analysis.

Selective serotonin reuptake inhibitors (SSRIs) are widely used for a variety of diseases, and their impact on semen quality is unclear. We performed a systematic search in PubMed and Embase, and after a strict screening, we included 4 studies with a total of 222 male participants. In result, SSRIs reduced normal sperm morphology (95% CI [-16.29, -3.77], p = 0.002), sperm concentration (95%CI [-43.88, -4.18], p = 0.02), sperm motility (95%CI [-23.46, -0.47], p = 0.04) and sperm DNA fragmentation index (DFI) (95% CI [6.66,21.93], p = 0.0002), without a statistically significant effect on semen volume (95%CI [-0.75,0.65], p = 0.89). Moreover, the impact on both sperm morphology and sperm concentration were observed within the 3-month period of SSRIs use. In general, our meta-analysis showed that SSRIs have a negative effect on semen quality. More larger, randomized, well-controlled clinical studies should be conducted to support our conclusion.