SOX2, SRY-box transcription factor 2, 6657

N. diseases: 503; N. variants: 23
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Our novel findings highlight the potential utility of miR-340-5p as a therapeutic agent for glioblastoma multiforme through inhibitory effects on Bcl-w-induced PDGF-A and Sox2 activation. 31272074 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE <b>Objective:</b> Our aim is to study the prognostic value of stem cell markers (CD44, Nestin, Olig2 and SOX2) in a series of homogeneously treated GBs. 31496301 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE NF inhibited the progression of GBM via the SOX2-AKT/STAT3-Slug signaling pathway. 30922391 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE The overexpression of ANGPTL4 induced GSC enrichment that was characterized by polycomb complex protein BMI-1 and SRY (sex determining region Y)-box 2 (SOX2) expression, resulting in TMZ resistance in GBM. 31717924 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE In addition, garcinol anticancer effect significantly attenuated the GBM stem cell-like phenotypes, as reflected by diminished ability of U87MG or GBM8401 to form colonies and tumorspheres and suppressed expression of OCT4 and SOX2. 31783691 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE ER stress and UPR activation in glioblastoma: identification of a noncanonical PERK mechanism regulating GBM stem cells through SOX2 modulation. 31534165 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Among all differentially expressed genes of GBM, CYGB (<i>r</i> = 0.5551; <i>P</i> < 0.0001), ISLR2 (<i>r</i> = 0.5126; <i>P</i> < 0.0001), RPP25 (<i>r</i> = 0.5333; <i>P</i> < 0.0001) and SOX2 (<i>r</i> = -0.4838; <i>P</i> < 0.0001) were strongly correlated with PLK2. 31763067 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Coculture of GAMs (and GAM-derived exosomes) and GBM cell lines increased GBM cells' resistance against temozolomide (TMZ) by upregulating the prosurvival gene programmed cell death protein 4 (PDCD4) and stemness markers SRY (sex determining region y)-box 2 (Sox2), signal transducer and activator of transcription 3 (STAT3), Nestin, and miR-21-5p and increasing the M2 cytokines interleukin 6 (IL-6) and transforming growth factor beta 1(TGF-β1) secreted by GBM cells, promoting the M2 polarization of GAMs. 31269723 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE qRT-PCR analysis was used to measure the expressions of miR-126-3p and SOX2 mRNA in GBM tissues and cells. 30980849 2019
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE The expression of FAT1, EMT (Snail/LOX/Vimentin/N-cad), stemness (SOX2/OCT4/Nestin/REST) and hypoxia markers (HIF-1α/VEGF/PGK1/CA9) was upregulated in ≥39% of GBM tumors (n = 31) with significant positive correlation (p ≤ 0.05) of the expression of FAT1 with LOX/Vimentin/SOX2/HIF-1α/PGK1/VEGF/CA9. 28994107 2018
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE The inhibition of switch genes highly correlates with the activation of genes related to neural development and differentiation, such as the 4-core OLIG2, POU3F2, SALL2, SOX2, whose induction has been shown to be sufficient to reprogram differentiated glioblastoma into stem-like cells. 30497369 2018
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE Our results also showed that metformin significantly suppressed self-renewal capacity of glioblastoma stem cells (GSCs), and expression of stem cell markers Bmi1, Sox2 and Musashi1, indicating that metformin can inhibit cancer stem-like properties of GBM cells. 29467947 2018
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE When HSF1 or BIS knockdown was combined with temozolomide (TMZ) treatment, a standard drug used in glioblastoma therapy, apoptosis increased, as measured by an increase in poly (ADP-ribose) polymerase (PARP) cleavage, whereas cancer stem-like properties, such as colony-forming activity and SOX2 protein expression, decreased. 28241425 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Finally, in the overexpression of AXL, EZH2 and Sox2 by transfection in GBM stem-like cells, we found that AXL/EZH2/TGF-ꞵ1, but not Sox2, might be a key regulator in tumor invasion, migration and EMT. 28208648 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Penfluridol treatment suppressed the phosphorylation of Akt at Ser473 and reduced the expression of GLI1, OCT4, Nanog and Sox2 in several glioblastoma cell lines in a concentration-dependent manner. 28380428 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE The immunofluorescence analysis of all cell cultures to evaluate the levels of SOX-2, a stemness marker aberrantly up-regulated in GBM, was also performed. 28424427 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE Moreover, CK suppressed the self-renewal capacity as well as the invasiveness of U87MG and U373MG GBM stem-like cells (GSCs) by inducing a reduction in the expression of GSC markers, such as CD133, Nanog, Oct4 and Sox2. 28656196 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Embryonic stem cell factors-OCT4, NANOG, and SOX2-contribute to the maintenance of stem cell properties and malignant progression in various cancers, including glioblastoma. 28933914 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Thus, FOXG1 and SOX2 operate in complementary but distinct roles to fuel unconstrained self-renewal in GBM stem cells via transcriptional control of core cell cycle and epigenetic regulators. 28465359 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Our findings suggest that miR-429 represents a potential tumour-suppressive miRNA and plays an important role in GBM progression by directly targeting SOX2. 28749077 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE Not all GBM cultures can generate GSCs, and this capacity is linked to >30% SOX2 levels. 28559081 2017
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE We further identified that metformin down-regulates SOX2 expression in TMZ-resistant glioma cells, reduces neurosphere formation capacity of glioblastoma cells, and inhibits GBM xenograft growth in vivo. 27791206 2016
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE CD9 silencing in three CD133+ glioblastoma cell lines (NCH644, NCH421k and NCH660h) led to decreased cell proliferation, survival, invasion, and self-renewal ability, and altered expression of the stem-cell markers CD133, nestin and SOX2. 26573230 2016
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 AlteredExpression disease BEFREE SOX2 and SOX9 expression correlates positively in glioma cells and glioblastoma biopsies. 26878385 2016
CUI: C1621958
Disease: Glioblastoma Multiforme
Glioblastoma Multiforme
0.100 Biomarker disease BEFREE Our results not only revealed the genetic plasticity contributing to drug resistance and stemness but also demonstrated the dominant role of SOX2 in maintenance of GBM CSCs, which may provide a novel therapeutic target to overcome the conundrum of poor survival of brain cancers. 27530866 2016