江西卫生职业学院

To examine the mechanism of action of tanshinone II A (Tan II A) in promoting chemosensitization of osteosarcoma cells to cisplatin (DDP). The effects of different concentrations of Tan II A (0–80 µ mol/L) and DDP (0–2 µ mol/L) on the proliferation of osteosarcoma cell lines (U2R, U2OS, 143B, and HOS) at different times were examined using the cell counting kit-8 and colony formation assays. Migration and invasion of U2R and U2OS cells were detected after 24 h treatment with 30 µ mol/L Tan II A, 0.5 µ mol/L DDP alone, and a combination of 10 µ mol/L Tan II A and 0.25 µ mol/L DDP using the transwell assay. After 48 h of treatment of U2R and U2OS cells with predetermined concentrations of each group of drugs, the cell cycle was analyzed using a cell cycle detection kit and flow cytometry. After 48 h treatment, apoptosis of U2R and U2OS cells was detected using annexin V-FITC apoptosis detection kit and flow cytometry. U2R cells were inoculated into the unilateral axilla of nude mice and then the mice were randomly divided into 4 groups of 6 nude mice each. The 4 groups were treated with equal volume of Tan II A (15 mg/kg), DDP (3 mg/kg), Tan II A (7.5 mg/kg) + DDP (1.5 mg/kg), and normal saline, respectively. The body weight of the nude mice was weighed, and the tumor volume and weight were measured. Cell-related gene and signaling pathway expression were detected by RNA sequencing and Kyoto Encyclopedia of Genes and Genomes pathway analysis. p38 MAPK signaling pathway proteins and apoptotic protein expressions were detected by Western blot. In vitro studies have shown that Tan II A, DDP and the combination of Tan II A and DDP inhibit the proliferation, migration and invasion of osteosarcoma cells. The inhibitory effect was more pronounced in the Tan II A and DDP combined treatment group (P<0.05 or P<0.01). Osteosarcoma cells underwent significantly cell-cycle arrest and cell apoptosis by Tan II A-DDP combination treatment (P<0.05 or P<0.01). In vivo studies demonstrated that the Tan II A-DD combination treatment group significantly inhibited tumor growth compared to the Tan II A and DDP single drug group (P<0.01). Additionally, we found that the combination of Tan II A and DDP treatment enhanced the p38 MAPK signaling pathway. Western blot assays showed higher p-p38, cleaved caspase-3, and Bax and lower caspase-3, and Bcl-2 expressions with the combination of Tan II A and DDP treatment compared to the single drug treatment (P<0.01). Tan II A synergizes with DDP by activating the p38/MAPK pathway to upregulate cleaved caspase-3 and Bax pro-apoptotic gene expressions, and downregulate caspase-3 and Bcl-2 inhibitory apoptotic gene expressions, thereby enhancing the chemosensitivity of osteosarcoma cells to DDP.

Abstract Purpose Fermitin family member 1 (FERMT1) is associated with the progression of different types of cancer. However, its biological functions of FERMT1 in prostate cancer (PC) are unclear. In this study, we preliminarily investigated the roles of FERMT1 and the mechanism by which it regulates the progression of PC. Methods The expression level of FERMT1 in PC tissues and cells was evaluated by immunohistochemical staining and Western blotting (WB) assay, respectively. Celigo cell count, cell counting kit-8 (CCK-8), flow cytometry, wound healing, Transwell assays and a mouse xenograft model was performed to evaluate the roles of FERMT1 in PC in vitro and in vivo. The interaction between p53 and FERMT1 was further investigated through co-immunoprecipitation (Co-IP). Finally, cells were treated with pifithrin-α (PFT-α), a p53 inhibitor, to investigate the regulatory role of p53 in the FERMT1-mediated progression of PC. Results FERMT1 was found to be upregulated in PC tissues and cells. Knocking down FERMT1 inhibited proliferation, migration, and cell cycle progression, and induced apoptosis in DU145 and LNCaP cell lines. Deleting FERMT1 also suppressed tumor growth of PC xenografts in vivo. More importantly, FERMT1 was discovered to play a significant role in cellular functions via the p53 signaling pathway, and the effects of FERMT1 knockdown on PC cellular function could be attenuated by pifithrin-α, a p53-inhibitor. Conclusions These findings of this study indicated that FERMT1 silencing partially inhibited PC progression via the p53 signaling pathway. Thus, FERMT1 is a promising potential therapeutic target for treating PC.

Objective To study the effect of ear cartilage in patients with nasal comprehensive plastic surgery. Methods Data were selected from 48 patients undergoing comprehensive nasal plastic surgery in our hospital from January 2019 to November 2021. The “differences in surgical materials” were divided into silicone group（silica gel, n=24） and research group（ear cartilage, n= 24）, the efficacy comparison between the two groups.Results There was no difference in clinical indicators between the two groups before treatment,P＞0.05; after treatment, compared with the control group, the observation group had lower nasolabial angles and nose bridge deflection angles, and higher nasal frontal angles and nose tip protrusions; surgery and hospitalization time were longer Short; the satisfaction rate of the observation group（95.83%） is higher than that of the control group（75.00%）, and the complication rate of the observation group（8.33%） is lower than that of the control group（33.33%）, χ~2=4.181,4547; P=0.041,0.033, P ＜0.05（statistically significant）.Conclusion The use of ear cartilage in the treatment of nasal comprehensive plastic surgery can improve the treatment, shorten the operation and hospitalization time, increase satisfaction, and reduce the occurrence of complications. It is worthy of praise.