Prostate cancer (PCa) is a common malignant tumor and the second leading cause of morbidity and mortality in men worldwide. Considering the prevalence and effects of PCa in males, an understanding of the molecular mechanisms underlying PCa tumorigenesis are essential and may provide novel therapeutic strategies for treating PCa. Bloom syndrome protein (BLM) is a member of the RecQ helicase family. The major function of BLM is to uncoil the double-stranded DNA structure. It has previously been demonstrated that BLM acts as a ‘genome caretaker’, and dysregulation of BLM function has been implicated in the development of multiple tumor types; however, its potential for inducing PCa tumorigenesis remains undetermined. The present study aimed to explore the function of BLM in PCa progression. Reverse transcription-polymerase chain reaction, immunohistochemistry and western blot analyses were performed to detect the BLM expression pattern in PCa patients and cell lines. The proliferation, and migration and invasion capacities of prostate cells were determined by EdU and Transwell assays following transfection with BLM-targeting short hairpin RNA (shRNA). The expression of BLM was significantly increased in PCa tissues and PC3 cells compared with non-PCa tissues and benign prostatic hyperplasia cells. Knockdown of BLM via shRNA inhibited PCa cell proliferation, and promoted PCa cell apoptosis. Notably, reducing the expression of BLM had no effect on the migration or invasive abilities of PCa cells. These results suggest that downregulation of BLM may alleviate PCa development, providing a novel perspective for PCa tumorigenesis and a potential therapeutic target for PCa.
Background Cognitive function in patients with primary hyperparathyroidism (PHPT) may be affected and be identified to have been linked to the level of parathyroid hormone (PTH). Previous studies have suggested that patients with PHPT present poor sleep quality, which might interact with cognitive decline. The purpose of this study was to determine whether sleep quality mediates the association between PTH level and cognitive function and investigate whether surgery improves sleep quality and cognition in PHPT patients. Methods Between June 2019 and August 2022, we recruited 146 patients diagnosed with PHPT (n = 146). We collected clinical data from medical records and evaluated sleep quality and cognition preoperatively and 2 months postoperatively by using the Pittsburgh Sleep Quality Index and Min-Mental State Examination. We examined the mediation effects of sleep disturbance and latency on correlations between PTH level and cognitive impairment by using the Bootstrap method. Results The sleep quality and cognitive function were correlated with PTH level before surgery. Sleep latency or sleep disturbance exhibited a partial mediating effect on the association between PTH level and MMSE scores in PHPT patients. (p < 0.05) In PHPT patients, there was a significant decline in PTH levels and an improvement in cognitive function post-surgery compared to pre-surgery, but no significant differences in sleep quality. Conclusion Sleep disturbance and sleep latency may mediate the association between PTH level and cognitive impairment in PHPT before surgery. The surgery could reduce PTH levels and improve cognition, but might not improve sleep quality in PHPT patients.
Bloom syndrome protein (BlM) is known to maintain genomic integrity including dna repair, recombination, replication and transcription. its dysregulation affects the genomic instability of cells, which results in a high risk of developing various types of cancer and even Bloom syndrome. However, to date, to the best of our knowledge, no association has been made between human BlM and bladder cancer. Thus, the aim of the present study was to investigate the role of BlM in human bladder cancer. The expression pattern of BlM in bladder cancer tissue was detected by immunohistochemistry. The viability, proliferation, cell cycle and apoptosis of bladder cancer cell lines were determined by Cell Counting Kit-8, EdU and flow cytometry following transfection of BlM small interfering rna. Finally, the effect of BlM on sensitivity of bladder cancer cell lines to cisplatin was investigated by reverse transcription-quantitative Pcr and western blot. it was demonstrated that the expression of BlM in human bladder cancer was increased compared with adjacent healthy bladder tissues. in addition, silencing of BlM inhibited the proliferation and promoted the apoptosis of bladder cancer cells and it also enhanced the sensitivity of bladder cancer cells to cisplatin. Together, the findings of the present study demonstrated that the regulation of BlM activity may have potential for use as a novel therapeutic target and a predictor for the prognosis of bladder cancer.
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