RESUMO
BACKGROUND: Prior studies have noted the importance of T cell immunoglobulin and mucin domain containing 4 (TIMD4) in various diseases and its functions on cell malignant behaviors. However, the biological function of TIMD4 in diffuse large B-cell lymphoma (DLBCL) is unknown. METHODS: Relative expression of TIMD4 was analyzed based on the GSE56315 array including 88 cases of human tissues. TIMD4 expression in cells was detected using a quantitative reverse transcriptase-polymerase chain reaction and western blot experiments. Cell proliferation was measured using the cell counting kit-8 (CCK-8) assay and apoptotic properties were assessed through the detection of related proteins by western blotting. The underlying molecular mechanism of TIMD4 in DLBCL was predicted and confirmed using KEGG enrichment analysis and western blotting. RESULTS: The results indicate that TIMD4 is overexpressed in DLBCL tissues and the poor prognosis of DLBCL patients is significantly linked with the higher TIMD4 expression. The loss-of-TIMD4 experiment in CYP6D reveals that knockdown of TIMD4 blocks cell growth and accelerates cell apoptosis, whereas the gain-of-TIMD4 experiment in Raji cells suggests that up-regulation of TIMD4 promotes cell proliferation and inhibits cell apoptosis. The activity of the Wnt/ß-catenin pathway is mediated by the TIMD4 expression in DLBCL cells. CONCLUSIONS: These findings demonstrate that TIMD4 is up-regulated in patients with DLBCL and the regulatory effects of TIMD4 on cell proliferation and apoptosis are associated with the Wnt/ß-catenin pathway, posing a novel target for DLBCL therapy.
Assuntos
Linfoma Difuso de Grandes Células B/patologia , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Via de Sinalização Wnt , Apoptose , Ciclo Celular , Linhagem Celular Tumoral , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Humanos , Linfoma Difuso de Grandes Células B/genética , Tonsila Palatina/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais , Regulação para CimaRESUMO
OBJECTIVE: Platelet-rich plasma (PRP) is extracted by centrifuging whole blood and characterized with a high concentration of platelets. The purpose of this systematic review and meta-analysis of randomized controlled trials (RCTs) and non-RCTs is to evaluate the efficacy and safety of platelet-rich plasma (PRP) versus placebo after total knee arthroplasty (TKA). METHODS: The Electronic databases of PubMed, Web of Science, Embase and Cochrane Database of Systematic Reviews were searched from inception to November 2016 and any studies involving PRP versus placebo for patients prepared for TKA were selected by two reviewers. The primary endpoint is the range of motion (ROM), which represents the function after TKA. The Western Ontario McMaster Universities Osteoarthritis Index Bellamy (WOMAC), pain at 24 h, 48 h and 7 day are also assessed the effect of PRP on the function and pain after TKA. The complications of infection is also compiled to assess the safety of PRP. Stata 12.0 was used to synthesis the final results. RESULTS: Eleven clinical trials with 1316 patients are included in the meta-analysis. The pooled results indicate that administration PRP significantly increase ROM on the third day (MD = 4.72, 95% CI 2.74, 6.69; P = 0.000) and 3 month postoperatively (MD = 7.55, 95% CI 5.91, 9.19; P = 0.000). There is no statistical difference between the two groups in terms of WOMAC questionnaire score in 3 months (MD = -4.88, 95% CI -12.12, 2.41; P = 0.190). There were no statistical significance between the two groups in pain intensity at 24 h, 48 h and 7 day. There is no statistically significant difference between the PRP versus placebo in terms of the occurrence of infection (RR = 0.64, 95%CI: 0.19-2.14, P = 0.464). CONCLUSION: Current meta-analysis indicates that PRP is associated with increasing the ROM after TKA in short term and long term. What's more, PRP can also decrease the WOMAC score and pain intensity without increasing the occurrence of infection.