ABSTRACT
Objective:To investigate the early and middle term clinical efficacies of 3D-printed metal prostheses in the reconstruction of bone defects after osteotomy in malignant bone tumors.Methods:A total of 34 patients with malignant bone tumors of lower extremity femur and tibia who underwent 3D printing individualized metal prosthesis replacement surgery in the Department of Bone and Soft Tissue of Affiliated Cancer Hospital of Zhengzhou University from March 2019 to March 2022 were retrospectively analyzed. There were 23 males and 11 females, with an average age of 19.1±15.2 years (range, 7-80 years). There were 22 children and adolescents younger than 18 years old. There were 3 cases in the proximal femur, 15 cases in the middle and distal femur, 10 cases in the proximal tibia and 6 cases in the distal tibia. According to the final pathological diagnosis, 24 cases of osteosarcoma, 6 cases of Ewing's sarcoma, 2 cases of undifferentiated sarcoma, 1 case of osteosarcoma, and 1 case of malignant giant cell tumor of bone were enrolled in this study. Postoperative complications, wound healing, periprosthetic fracture and aseptic loosening, tumor outcome (evaluated by tumor control evaluation criteria), and length difference of lower limbs were recorded. Response evaluation criteria in solid tumor (RECIST) was used to evaluate tumor outcomes. Prosthetic-bone interface healing was evaluated postoperatively, and the function was evaluated based on Musculoskeletal Oncology Society (MSTS) 93.Results:The length of lesions was 70-240 mm in 34 patients, with an average of 125.5±35.4 mm. The length of osteotomy was 80-275 mm, with an average of 160.2±33.9 mm. No tumor was found on the osteotomy surface. The customized prosthesis was firmly installed and closely matched with the side of the preserved articular surface. There were 2 patients with local incision fat liquefaction and 4 patients with superficial wound infection, which healed after debridement and antibiotic treatment. One distal tibia osteosarcoma case developed severe periprosthetic infection 2 months after surgery, resulting in prosthesis implantation failure, limb movement pain and poor ankle function. After removal of the prosthesis, infection control and osteogenesis with the Ilizarov technique, the infection was completely controlled and local osteogenesis was possible. The remaining 33 patients had a good prosthetic-bone interface union. One case was found to have localized bone resorption on the contact surface of the prosthesis 7 months after operation, but the metal prosthesis and screws were not loose. The incisions healed well in other patients, without infection, prosthesis loosening, fracture or other complications. All patients survived and were followed up for 13.8±5.6 months (range, 7-27 months). During the follow-up, there was no recurrence of tumor at the osteotomy end in all patients, but 5 patients developed lung metastasis. At the end of the last follow-up, all patients survived. Among them, 16 patients had unequal length of lower limbs, including 10 cases within 2 cm, 3 cases between 2-5 cm, and 3 cases over 5 cm. With the exception of one patient whose prosthesis was removed due to infection, the MSTS 93 of the other patients was 24.9±2.2 (range, 19-28), and were rated as excellent in 26 cases and good in 7 cases. According to the RECIST evaluation criteria, 26 of 34 patients had complete response, 5 had disease progression, and 3 had stable disease.Conclusion:3D printed metal prosthesis is one of the effective methods for the treatment of bone defects after resection of malignant bone tumors in lower limbs, which is safe, reliable and has satisfactory early curative effect.
ABSTRACT
Objective:To evaluate the effect of propofol on proliferation, invasion and migration of human melanoma cells and role of cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2)/matrix metalloproteinase (MMP) signaling pathway.Methods:SKMEL-5 cells were cultured in vitro and divided into 4 groups ( n=36 each) using the random number table method: control group (group C), propofol group (group P), COX-2 overexpression group (group COX-2), and COX-2 overexpression plus propofol group (group COX-2+ P). Propofol at the final concentration of 60 μmol/L was added in group P. The COX-2 overexpression plasmid pcDNA3.1-COX-2 was transfected into SKMEL-5 cells in group COX-2 and group COX-2+ P, and propofol at the final concentration of 60 μmol/L was added in group COX-2+ P.After incubation for 48 h, the cell proliferation rate was determined by CCK-8 method, the cell invasion and migration ability was determined by Transwell assay, the expression of COX-2 in cells was detected by Western blot, the expression of COX-2 mRNA in cells was detected by quantitative real-time polymerase chain reaction, and the concentrations of serum PGE2, MMP-2 and MMP-9 were determined by enzyme-linked immunosorbent assay. Results:Compared with group C, the cell proliferation rate was significantly decreased, the number of cell invasion and migration was decreased, the expression of COX-2 protein and mRNA was down-regulated, and the concentrations of PGE2, MMP-2 and MMP-9 in the supernatant were decreased in group P, and the cell proliferation rate was significantly increased, and the number of cell invasion and migration was increased, the expression of COX-2 protein and mRNA was up-regulated, and the concentrations of PGE2, MMP-2 and MMP-9 in the supernatant were increased in group COX-2 ( P<0.05). Compared with group P, the cell proliferation rate was significantly increased, and the number of cell invasion and migration was increased, the expression of COX-2 protein and mRNA was up-regulated, and the concentrations of PGE2, MMP-2 and MMP-9 in the supernatant were increased in group COX-2+ P ( P<0.05). Conclusions:Propofol can inhibit the proliferation, invasion and migration of human melanoma cells, and the mechanism may be related to inhibition of the COX-2/PGE2/MMP signaling pathway.
ABSTRACT
PURPOSE: Long non-coding RNA taurine upregulated gene 1 (TUG1) is reported to be a vital regulator of the progression of various cancers. This study aimed to explore the exact roles and molecular mechanisms of TUG1 in osteosarcoma (OS) development. MATERIALS AND METHODS: Real-time quantitative PCR was applied to detect the expressions of TUG1 and microRNA-132-3p (miR-132-3p) in OS tissues and cells. Western blot was performed to measure protein levels of sex determining region Y-box 4 (SOX4). Cell viability was assessed using XTT assay. Cell apoptosis was evaluated using flow cytometry and caspase-3 activity detection assays. Bioinformatics analysis and luciferase reporter experiments were employed to confirm relationships among TUG1, miR-132-3p, and SOX4. RESULTS: TUG1 was highly expressed in human OS tissues, OS cell lines, and primary OS cells. TUG1 knockdown hindered proliferation and induced apoptosis in human OS cell lines and primary OS cells. Moreover, TUG1 inhibited miR-132-3p expression by direct interaction, and introduction of miR-132-3p inhibitor partly abrogated the effect of TUG1 knockdown on the proliferation and apoptosis of OS cells. Furthermore, SOX4 was validated as a target of miR-132-3p. Further functional analyses revealed that miR-132-3p inhibited proliferation and induced apoptosis of OS cells, while this effect was greatly abated following SOX4 overexpression. Moreover, TUG1 knockdown suppressed proliferation and promoted apoptosis by upregulating miR-132-3p and downregulating SOX4 in primary OS cells. CONCLUSION: TUG1 facilitated proliferation and suppressed apoptosis by regulating the miR-132-3p/SOX4 axis in human OS cell lines and primary OS cells. This finding provides a potential target for OS therapy.