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Sushi repeat‐containing protein X‐linked 2 (SRPX2), a novel chondroitin sulfate proteoglycan, is reported to play a critical role in tumorigenesis. However, the expression and functional role of SRPX2 in prostate cancer have not been defined. Thus, the aim of this study was to investigate the expression and functional role of SRPX2 in human prostate cancer. Our results showed that the expression of SRPX2 was obviously increased in human prostate cancer tissues and cell lines. In addition, knockdown of SRPX2 inhibited the proliferation, migration, and invasion of prostate cancer cells, as well as prevented the epithelial‐mesenchymal transition process in prostate cancer cells. Mechanically, knockdown of SRPX2 efficiently inhibited the activation of PI3K/Akt/mTOR pathway in prostate cancer cells. Taken together, these data demonstrated that knockdown of SRPX2 inhibits the proliferation and metastasis in human prostate cancer cells, partly through the PI3K/Akt/mTOR signaling pathway. Thus, SRPX2 may be a novel therapeutic target for the treatment of prostate cancer. [ABSTRACT FROM AUTHOR]

Background: Osteoking (OK) is prescribed in traditional Chinese medicine to accelerate fracture healing. Although some studies suggest the potential efficacy of OK for fracture healing, the evidence remains inconclusive., Aim: To systematically evaluate the safety of OK and its effect on fracture healing., Methods: Relevant authoritative databases were searched until 25 August 2023. Randomized controlled trials (RCTs) of patients with fractures treated with Osteoking were included. We evaluated the risk of bias using the Cochrane tool and performed a meta-analysis using the Review Manager 5.4 software package., Results: 13 studies involving 1123 participants were included. This meta-analysis showed that compared with observations in the control group, the OK group showed a shortened fracture healing time, increased fracture healing rate, reduced swelling regression time and ecchymosis regression time, and improved bone metabolism. In addition, the included studies did not report any serious side effects associated with the use of OK, and the mild side effects resolved without treatment., Conclusion: OK therapy is beneficial and safe for accelerating fracture healing, reducing swelling, eliminating ecchymosis, and improving bone metabolism. However, the meta-analysis results do not support OK treatment for improving the fracture healing rate at all fracture sites and reducing pain across all fracture sites. Further original, high-quality studies are needed to validate these findings., Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=452430, identifier CRD42023452430., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhang, Kuang, Zhang, Rong, Yuan, Peng, Zhao, Liu, Ou and Kuang.)

Aims: Vascular calcification is a major risk factor for cardiovascular mortality accompanied by DNA damage. Cyclic GMP-AMP synthase (cGAS) is a DNA sensor that is activated by genomic DNA damage. Here, we investigated the molecular mechanisms linking cGAS to vascular calcification., Main Methods: Diabetic arteriosclerotic model and vascular calcification of primary vascular smooth muscle cells (VSMCs) were induced. Calcification was visualized with Alizarin red staining. Calcium deposition and alkaline phosphatase activity were analyzed by respectively kits. Deacetylation of cGAS was investigated using co-immunoprecipitation assay., Key Findings: Protein, but not mRNA, expression of cGAS is down-regulated in VSMCs and animal models of calcification. Overexpression of cGAS attenuated high-Pi induced calcification, calcium content and ALP activity. In addition, cGAS regulated VSMCs phenotype as overexpression of cGAS increased expression of contractile markers α-SMA and SM22α and decreased the expression of osteogenic markers RUNX2 and BMP2. The LC3II/LC3I ratio and Atg5 level were upregulated by cGAS overexpression. Under calcification-inducing conditions, HDAC1 deacetylates cGAS and inactivates it. HDAC1 knockdown by short hairpin HDAC1 reversed the cGAS-induced reduction in vascular calcification, as well as in autophagy., Significance: HDAC1-induced cGAS deacetylation enhances vascular calcification and may therefore be a potential therapeutic target., Competing Interests: Declaration of competing interest The authors declare that there is no conflict of interests., (Copyright © 2018. Published by Elsevier Inc.)

Sushi repeat-containing protein X-linked 2 (SRPX2), a novel chondroitin sulfate proteoglycan, is reported to play a critical role in tumorigenesis. However, the expression and functional role of SRPX2 in prostate cancer have not been defined. Thus, the aim of this study was to investigate the expression and functional role of SRPX2 in human prostate cancer. Our results showed that the expression of SRPX2 was obviously increased in human prostate cancer tissues and cell lines. In addition, knockdown of SRPX2 inhibited the proliferation, migration, and invasion of prostate cancer cells, as well as prevented the epithelial-mesenchymal transition process in prostate cancer cells. Mechanically, knockdown of SRPX2 efficiently inhibited the activation of PI3K/Akt/mTOR pathway in prostate cancer cells. Taken together, these data demonstrated that knockdown of SRPX2 inhibits the proliferation and metastasis in human prostate cancer cells, partly through the PI3K/Akt/mTOR signaling pathway. Thus, SRPX2 may be a novel therapeutic target for the treatment of prostate cancer., (© 2018 Wiley Periodicals, Inc.)