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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
Several studies have claimed that SOX4 plays an essential part in cell activities, such as Li et al. [30] proved that through upregulating SOX4 expression, the proliferation, migration, and invasion of ovarian cancer cells were promoted. Another research confirmed that SOX4 was a functional target of miR-132 in lung cancer cells and liver cancer cells [17,19]. Furthermore, Sun et al. [20] claimed that SOX4 was upregulated in CC cells and was an unfavourable biomarker of malignant status in CC. On the basis of these studies, we discovered that miR-132 expression was negatively correlated with SOX4, and overexpression of miR-132 reduced SOX4 level and inhibited the proliferation, invasion, migration, and EMT process of CC cells, while these results were reversed by SOX4 overexpression. More interestingly, we found that co-transfection of miR-132 and pcDNA-SOX4 seemed to overcome the downregulation of intrinsic SOX4 by miR-132 mimic, implying that expression of SOX4 from pcDNA-SOX4 was not affected by miR-132, and miR-132 only downregulated expression of intrinsic but not extrinsic SOX4 in the cells. The probably reason is that pcDNA-SOX4 vector do not contain the 3′-UTR, and it can upregulate SOX4 but cannot be degraded by miR-132 mimic when transfected into the cells. Importantly, there are some researches perform the recure experiments like us and show the similar results, such as the studies of Yang et al. [31], Li et al. [32] and Geng et al. [33], which can in favour of our results.
Serum Based miRNA as a Diagnostic Biomarker for Multiple Sclerosis: a Systematic Review and Meta-Analysis
Published in Immunological Investigations, 2022
Samar A. Zailaie, Jumana Jamal Siddiqui, Rawan Mansour Al Saadi, Dalia Mohammad Anbari, Amani S. Alomari, Edward James Cupler
In the progressive phenotype of the disease, our review found that miR-191-5p tends to be the most significant deregulated miRNAs among PPMS patients in comparison to other MS types. Only one study by Vistbakka et al has reported a diagnostic value for miR-191-5p in PPMS of 80% with a sensitivity of 74% and specificity of 81% in comparison to SSPM. Another study by Vistbakka et al reported the same expression direction miR-191-5p in an independent cohort. However, this miRNA was not counted for the meta-analysis due to the unavailability of the other study reporting the values required for the quantitative analysis. In normal appearing white matter (NAWM), a decreased expression of miR-191-5p has been found to correlate with CNS inflammatory response (Guerau-De-Arellano et al. 2015). Guerau-de-Arell et al predicted SOX4 mRNA as a potential target for miR-191-5p along with other genes involved in CNS homeostasis. A high expression of SOX4 has been reported to inhibit oligodendrocyte differentiation and knockdown of SOX4 protein increased maturation process of glia into neurons (Braccioli et al. 2018). The PPMS phenotype characterized by a progressive neurological dysfunction with more axonal damage accumulation and neurodegeneration than other MS phenotype. Loss of miR-191-5p expression seen in PPMS could enhance SOX4 expression and prevent myelination leading to more axonal damage and neurons death. Giving the vital role of miR-191-5p in re-myelination and OL differentiation, it could be used as a potential predictor for PPMS aiding in its diagnosis (Petzold et al. 2005).