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Percutaneous Nephrolithotomy (PCNL) and Retrograde Intrarenal Surgery (RIRS) are widely used in the management of kidney stones. But the safety and efficiency between these two technologies is still a mystery. This meta-analysis was performed to compare the efficacy as well as safety of Minimally Invasive Percutaneous Procedures (MIPPs) including ultra mini-PCNL, mini-PCNL, and micro-PCNL with RIRS. PubMed, Embase and Scopus were searched, and twelve studies included data on 1207 cases (613 for MIPPs and 594 for RIRS) satisfied the inclusion criteria and were included in this research finally. MIPPs were found to be associated with higher stone-free rate but longer hospital stays, and a larger drop in hemoglobin levels. Difference between MIPPs and RIRS in complication rate, operative time, and total cost were not notable. Given no obvious difference in the complication rate and higher efficacy, our findings suggest that mini-PCNL should be recommended over RIRS for stones>2 cm, and that for stones<2 cm any of MIPPs or RIRS are reasonable.

Purpose: To investigate the clinical relevance and biological function of the kinesin super-family protein 4A (KIF4A) expression in prostate cancer (PCa). Methods: We examined 1) the relationship between the expression of KIF4A and clinico-pathological characteristics of PCa patients using a tissue microarray and the Cancer Genome Atlas database, 2) the prognostic value of KIF4A expression in patients using Kaplan-Meier plots and 3) the functions of KIF4A in LNCaP and DU145 cells, such as cell proliferation, cell cycle and cell apoptosis. Results: Compared with normal prostate, the mRNA and protein expressions of KIF4A were up-regulated in PCa. The up-regulation expression rates of KIF4A in PCa were significantly related to the Gleason score (P

Metformin is a classic type II diabetes drug which possesses anti-tumor properties for various cancers. However, different cancers do not respond to metformin with the same effectiveness or acquire resistance. Thus, searching for vulnerabilities of metformin-resistant prostate cancer is a promising strategy to improve the therapeutic efficiency of the drug. A genome-scale CRISPR-Cas9 activation library search targeting 23,430 genes was conducted to identify the genes that confer resistance to metformin in prostate cancer cells. Candidate genes were selected by total reads of sgRNA and sgRNA diversity, and then a CCK8 assay was used to verify their resistance to metformin. Interestingly, we discovered that the activation of ECE1, ABCA12, BPY2, EEF1A1, RAD9A, and NIPSNAP1 contributed to in vitro resistance to metformin in DU145 and PC3 cell lines. Notably, a high level of RAD9A, with poor prognosis in PCa, was the most significant gene in the CCK8 assay. Furthermore, we discerned the tumor immune microenvironment with RAD9A expression by CIBERSORT. These results suggested that a high level of RAD9A may upregulate regulatory T cells to counterbalance metformin in the tumor immune microenvironment.

Objective: To investigate the effect of PBK on cell cycle and apoptosis of prostate cancer cell lines.Methods: Obtain the differences expression gene, PBK, which related to prostate cancer from high-throughput microarray, Furthermore, the cell cycle and apoptosis of prostate cancer cells were detected by flow cytometry after transfection with PBK inhibitor and overexpression plasmid.Results: After DU145/LNCaP transfection, the PBK expression levels were measured at 48 hours by RT-qPCR, compared to the blank control groups, the data showed the expression of PBK was significantly decreased in the groups of Si-PBK cell lines (DU145, the inhibition rate=84.78% P<0.01; LNCaP, the inhibition rate=94.79%, P<0.01); While the expression of PBK was significantly increased in the overexpression groups (DU145, fold=1.20, P<0.05; LNCaP, fold=1.35, P<0.05). The results of cell cycle analysis showed that after inhibition of the expression of PBK caused cell cycle arrest at the G0/G1 phase (LNCaP, P<0.05; DU145, P<0.01); On the contrary, a higher proportion of S, G2/M phase was shown in the over-expression-PBK DU145/LNCaP cell lines (LNCaP, P<0.05; DU145, P<0.01). Lastly, the cell apoptosis of DU145 and LNCaP cells was significantly increased after the inhibition of PBK expression (P<0.05) while an opposite result shown in the PBK overexpression cell lines (LNCaP, P<0.01; DU145, P<0.05). Conclusion: PBK can shorten the cell cycle and inhibit apoptosis of prostate cancer cells, which indicates that PBK can sever as a tumor promoter in prostate cancer. technology to carry out gene detection in 5 cases of PCa patients in