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Definition, risk factors, and epidemiology of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
New candidates associated with BMD have also been suggested, including wntless Wnt ligand secretion mediator (GPR177) genes, and SRY-box 6 (SOX6), a transcriptional activator that is required for normal development of chondrogenesis and maintenance of skeletal muscle cells (73). A panel of more than 25 genes has been associated with BMD by GWAS analysis in postmenopausal women, including ARHGAP1, CLCN7, CTNNB1, ESR1, FAM3C, FLJ42280, FOXL1, GALNT3, GPR177, HDAC5, IBSP, JAG1, LRP5, LTBP3, MARK3, MEF2C, MEPE, OPG, RANK, RANKL, RSPO3, SOST, SOX4, SOX6, SP7 (Osterix), TARD3NL, and ZBTB40 (74).
High-Dimensional, Penalized-Regression Models in Time-to-Event Clinical Trials
Published in Susan Halabi, Stefan Michiels, Textbook of Clinical Trials in Oncology, 2019
Federico Rotolo, Nils Ternès, Stefan Michiels
The clinico-genomic prediction model, established through the model in Equation 18.11 subject to the adaptive lasso penalty, can be found in Ternès et al. [48]. This model contains 102 prognostic variables (four clinical and 98 genomic variables) and 24 treatment-effect modifiers. Interestingly, some prognostic biomarkers had already been identified in the biomedical literature, e.g., SOX4 [55] or CSNK1D [56]. Some immune genes were also identified in the treatment-effect modifying component, which is consistent with some articles highlighting the involvement of immune pathways in the efficacy of trastuzumab.
MicroRNA-320a-containing exosomes from human umbilical cord mesenchymal stem cells curtail proliferation and metastasis in lung cancer by binding to SOX4
Published in Journal of Receptors and Signal Transduction, 2022
The decline of miR-320a in exosomes occurred concomitant with the promotion of SOX4 in the present study. Bioinformatics analysis displayed that the SOX4 3’UTR harbors potential binding sites for miR-320a, and luciferase reporter assays validated that SOX4 is a possible target of miR-320a. SOX4 is found to be necessary for the process of epithelial-mesenchymal transition, migration and metastatic spread [15]. In addition, miR-129-5p repressed cell proliferation, migration and induced apoptosis by targeting SOX4 and modulating the Wnt/β-catenin pathway in chondrosarcoma [36]. Meanwhile, miR-320a downregulation prohibited liver cancer cell from proliferation via the Wnt/β‑catenin pathway [37]. Glioma cells co-cultured with exosomes carrying miR-133b mimic demonstrated reduced protein expression of Wnt1 and β-catenin, while the opposite trends were observed in cells treated with exosomes containing miR-133b inhibitor [38], which was consistent with the obtained data from our research. Accordingly, lung cancer cells co-cultured with exosomes were further introduced with the β-catenin-specific agonist WAY-262611, and the repressive role of exosomes on lung cancer progression was reversed. In line with our observations, the Wnt/β-catenin pathway inhibitor IWP-2 was found to halt cell proliferation and potentiate cell apoptosis, and could counteract the stimulative role of SOX9 in lung cancer cell proliferation [39], implying the possible interaction between SOX4 and the Wnt/β-catenin pathway in lung cancer.
LncRNA SNHG5 promotes cervical cancer progression by regulating the miR-132/SOX4 pathway
Published in Autoimmunity, 2021
Liqin Zhang, Xiaoming Wu, Yue Li, Xianlin Teng, Libo Zou, Beiwei Yu
Previous research demonstrated that SNHG5 expression was increased in colorectal cancer tissues and cells, which promoted cell proliferation, metastasis, and migration through regulating miR-132-3p [16]. In our study, we firstly discovered SNHG5 was highly expressed in CC tissues (Figure 1(A)). Then, we detected the miR-132 expression and SOX4 mRNA level using qRT-PCR. Results showed that miR-132 expression was decreased and SOX4 mRNA level was increased in CC tissues (Figure 1(B)). The protein level of SOX4 was augmented in tumour tissues compared with adjacent tissues (Figure 1(C)). Pearson’s correlation analysis indicated that in CC tissues, the expression of SNHG5 was positively correlated with SOX4 expression, and the expression of miR-132 was negatively correlated with SNHG5 and SOX4 expressions (Figure 1(D)). In SiHa and ME-180 cells, the expression of SNHG5 and SOX4 was increased, and the expression of miR-132 was decreased compared with Ect1/E6E7 cells (Figure 1(E–G)). According to the average value of SNHG5 level in CC patients, we assigned the patients into low SNHG5 level group (n = 19) and high SNHG5 level group (n = 21). Patient characteristics between the low SNHG5 expression and the high SNHG5 expression group were shown in Table 1. SNHG5 high expression had a positive correlation with FIGO stage (p = .003) and lymph node metastasis (p = .001).
LncRNA TDRG1 promotes the proliferation, migration, and invasion of cervical cancer cells by sponging miR-214-5p to target SOX4
Published in Journal of Receptors and Signal Transduction, 2020
Meijun Guo, Beibei Lin, Guoping Li, Jun Lin, Xiuxiu Jiang
TargetScan7.2 predicted that SOX4 was the target gene of miR-214-5p (Figure 8(A)), and the prediction was verified by dual-luciferase reporter assay (Figure 8(B,C)), as a significantly low luciferase activity was observed in the siNC group in both HeLa and SiHa cells (p < 0.001). The expression of SOX4 in normal and CC tissues was also measured (Figure 8(D)), and we found that SOX4 expression was significantly high in CC tissues (p < 0.001). Moreover, the expression of SOX4 in transfected HeLa and SiHa cells was determined (Figure 8(E,F)), and the results showed that expression of SOX4 was greatly low in siTDRG1 in both CC cells, while it was the most high-expressed in miR-214-5p inhibitor groups. Moreover, compared with siTDRG1 group, the expression level of SOX4 was increased by siTDRG1 and miR-214-5p inhibitor (p < 0.001).