Whereas, overexpression of microRNA‑152 targets DKK1 to inhibit cell proliferation, induce apoptosis, and promote LDH activity, caspase-3/9 activities and Bax/Bcl-2 and p53 protein expression levels of osteosarcoma through inactivation of the Wnt/β-catenin signaling pathway.
Pediatric oncologists were e-mailed an anonymous 18-question survey assessing their willingness to offer TP53 germline testing to a child with osteosarcoma with or without a family history, and they were evaluated for changes in their choices with the prior data and the new data.
A rearranged signal was found in 20/37 cases (54%) of OS and in none of the other sarcomas or benign bone lesions, giving the FISH test 100% specificity for a diagnosis of OS. p53 immunostaining was generally not predictive of the results obtained by FISH and could not substitute for this test.
In current study, we evaluated the relationship between genetic variation of the p53 binding site and the OS susceptibility through a two-stage case-control study in Chinese population.
High TACC3 expression was observed in 19 of 33 osteosarcoma specimens (58%), and this was associated with larger tumor size (ie, AJCC stage IIB in this study; p = 0.002), higher p53 expression (p = 0.007), and higher Ki-67 expression (p = 0.002).
Topological analysis of the OSM identified 11 genes, including APP, APPBP2, ATXN1, HSP90B1, IKZF1, KRTAP10-1, PAK1, PDPK1, SMAD4, SUZ12 and TP53 as potential diagnostic biomarkers for osteosarcoma.
In summary, these findings demonstrate the oncogenic role of SFRP2 in the development of p53 mutation-associated OS and that inhibition of SFRP2 is a potential therapeutic strategy.
Overexpression of microRNA-381 using microRNA-381 mimics inhibited cell proliferation, induced apoptosis and increased LDH activity, caspase‑3/9 activities, expression of Bax/Bcl-2 and p53 protein in osteosarcoma of in vitro model through downregulation of LRH-1/Wnt/β-catenin signaling pathway.
Exposure to radiation induces osteosarcoma cell apoptosis by upregulation of p53 both in U2OS (p53-wt) and exogenous p53-introduced MG-63 (p53-null) osteosarcoma cells.
This study warrants a future evaluation of this formulation for gene silencing efficiency of mutant p53 in tissue culture and animal models for the treatment of osteosarcoma.
Three genes, CD137L, CDC42 binding protein kinase gamma and Follistatin, were identified as novel direct p53 target genes that exhibited growth-suppressive effects on osteosarcoma cell lines.
1847-1857) develop a new mouse model of osteosarcoma in which a GOF mutant p53 allele is expressed specifically in osteoblasts, while the tumor microenvironment remains wild type for p53, allowing for the study of cell-autonomous functions.
The results indicated that p53 protein expression was not linked to age factor, gender, tumor grade, cancer metastasis and response to chemotherapy. p53 expression was significantly lower in osteogenic osteosarcoma than in nonosteogenic osteosarcoma (OR = 0.40; p = 0.006). p53 expression was associated with a poor prognosis of patients in overall survival (univariate analysis: HR: 2.49; p < 0.001 and multivariate analysis: HR: 2.92; p < 0.001).
Synthesized molecules were evaluated for their ability to induce apoptosis in two cancer cell lines and their derivatives with different status of p53 (colorectal HCT116 and osteosarcoma U2OS cells) by Annexin V staining.
The expression of mutant p53 protein in 65 cases of osteosarcoma was detected by immunohistochemistry to analyze the correlation between p53 and the development of osteosarcoma. qPCR showed that WWOX and p53 mRNA was overexpressed in MW and MP cells, respectively.
Microarray and p53 chromatin immunoprecipitation combined with sequencing (ChIP-seq) datasets of the OS cell line U2OS treated with distinct drugs were acquired from the Gene Expression Omnibus and differentially-expressed genes (DEGs) were screened for alignment analysis.
Thus, in mouse tumors with high frequency of p53 LOH (osteosarcomas and fibrosarcomas), we find that mutant p53 protein is stabilized (16/17 cases, 94%) and tumor onset is significantly accelerated compared with p53+/- tumors (GOF).
Tumor protein p53 (TP53), mitogen-activated protein kinase 1 (MAPK1) and estrogen receptor 1 (ESR1) were identified the most important osteosarcoma‑associated genes, with the highest levels of topological properties.