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Sox7 promotes tumor growth via vessel abnormalization, and its level determines the therapeutic outcome of VEGFR2 inhibition in High-grade glioma.
Our findings demonstrated that SOX7 methylation conferred adverse prognosis in myelodysplastic syndrome patients and was associated with leukemia progression.
MiR-494-3p promotes nasopharyngeal carcinoma cell growth, migration, and invasion by directly targeting Sox7.
These results provide the first clue that miR-24-3p could play a role as an oncomiR in Lung cancer by regulating SOX7.
we have identified an array of potential target genes of SOX7 and examined four of them for their roles in SOX7-mediated tumor suppression. We found that SOX7 could both activate and repress its target genes; and achieve its antiproliferative function through regulating multiple genes simultaneously.
SOX7 transcription factor mediates PDGF-BB-induced IL-33 expression.
Mechanistically, SOX7 was confirmed to be the downstream target of miR-616 in NSCLC cells. Forced expression of SOX7 prevented the promoting effects of miR-616 overexpression on the proliferation and metastasis of NSCLC cells, while knockdown of SOX7 reversed the inhibitory effects of miR-616 knockdown on the proliferation and metastasis of NSCLC cells.
miR-9 was up-regulated and SOX7 was down-regulated in human non-small-cell lung cancer tissues and cell lines.
The results indicate that SOX7 may inhibit the progression of liver carcinoma and that SOX7 downregulation may accurately predict poor prognosis in liver carcinoma patients.
Consistent with bioinformatics predictions, SOX7 was correlated positively with AXIN2 and negatively with beta-catenin, suggesting that SOX7 and AXIN2 might play important roles as co-regulators through the Wnt-beta-catenin pathway in the breast tissue to affect the carcinogenesis process.
SOX7 inhibits oncogenic beta-catenin-mediated transcription by disrupting the beta-catenin/BCL9 interaction.
Overexpression of miR-935 inhibited SOX7 expression.
The results suggest that miR-664 functions as an oncogene miRNA and has an important role in promoting human osteosarcoma cell invasion and migration by suppressing SOX7 expression.
miR-595 played a critical role in carcinogenesis by suppression of SOX7.
Aberrant methylation of the promoter regions of the SOX7 gene in patients with acute myeloid leukemias.
miR-935 contributed to cell proliferation of gastric cancer through targeting SOX7.
the HMG-box is a key domain of SOX7 for negatively regulating the Wnt/beta-catenin signaling pathway when functioning as a tumor suppressor in a glioma.
The results provided unequivocal evidence for a novel tumor suppressor role of SOX7 in acute myeloid leukemia
SOX7 plays an important inhibitory role in hepatocarcinogenesis, and might be a novel target for hepatocellular carcinoma therapy.
Ectopic expression of miR-492 led to downregulation of SOX7 protein.
Data show that SOX7, SOX17 and SOX18 (SOXF) transcriptional factors are induced during satellite cell specification.
SOX7 is dispensable for myogenesis but is necessary to promote satellite cell development and survival.
By E10.5, both Sox7 complete knockout and FLK1-specific deletion of Sox7 lead to widespread vascular defects. In contrast, while SOX7 is expressed in the earliest specified blood progenitors, the VAV-specific deletion of Sox7 does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 in vasculogenesis and angiogenesis during embryonic development.
Data provide evidence that the uncontrolled expression of the transcription factor SOX7 in adult haematopoietic cells has dramatic consequences on blood homeostasis with alterations of the haematopoietic system, inducing the proliferation of blood progenitors in the bone marrow while blocking B lymphopoiesis.
SOX7 inhibits the expression of RUNX1 target genes in hemogenic endothelium, while having no effect on RUNX1 expression itself. SOX7 directly interacts with RUNX1 and inhibits its transcriptional activity.
Dynamically and epigenetically coordinated GATA2/ETS1SOX7 transcription factor expression is indispensable for endothelial cell differentiation.
combined deletion of Sox7, Sox17, and Sox18 at the onset of retinal angiogenesis leads to a dense capillary plexus with a nearly complete loss of radial arteries and veins, whereas the presence of a single Sox17 allele largely restores arterial identity
These data indicate that Sox7 is dispensable for both differentiation and maturation of primitive endoderm in an mouse embryonic stem cell model system.
ETV2 directly regulates Sox7, and ETV2 governs endothelial development by regulating transcriptional networks which include Sox7.
Notch and SoxF factors combinatorially regulate Dll4 expression in arteries downstream of VEGF.
Haploinsufficiency of Sox7 or Gata4 is sufficient to produce anterior congenital diaphragmatic hernia in mice.
Disrupted SOXF function results in epidermolysis bullosa-like skin phenotypes.
SOX7 regulates the expression of VE-cadherin in the haemogenic endothelium at the onset of haematopoietic development.
Sox7-sustained expression in the earliest committed hematopoietic precursors promotes the maintenance of their multipotent and self-renewing status.
SOX7 and GATA-4 are competitive activators of Fgf-3 transcription
SOX7 and SOX17 bound specifically to two SOX-binding sites within the Lama1 enhancer, and that these SOX-binding sites functioned synergistically to confer the trans-activation by SOX7 and SOX17
is required for the induction of Gata-4 and Gata-6, and the interplay among these transcription factors plays a crucial role in parietal endoderm differentiation
differential Sox7 gene expression presents a novel biomarker profile, and possible regulatory switch, to distinguish cardiovascular pedigrees within Flk-1(+) multi-lineage progenitors
both Sox7 and Sox15 are able to induce the early stages of myogenesis.
Sox7 levels are crucial in arterial specification in conjunction with hey2 and efnb2 function, with mutants in all three genes displaying shunt formation and an arterial block.
Sox7/18 factors and Notch regulate nr2f2 gene expression during venous differentiation in zebrafish.
Sox7 and Sox18-mediated transcriptional regulation of Robo4 is important in the developing embryonic vasculature
Sox7 and sox18 are specifically expressed in the developing vasculature, and simultaneous loss of their function results in a severe loss of the arterial identity of the presumptive aorta.
Sox7 and sox18 play redundant but collectively essential roles in the establishment of proper arteriovenous identity in zebrafish.
Sox7 and Sox18 control arterial-venous identity by regulating Gridlock expression.
SOX7 mRNA is localized to the vegetal region of the blastula-stage embryo
SOX7 and SOX18b are essential regulators of cardiogenesis in Xenopus.
Vegetal pole localized Sox7 positively regulates Nodal (Xnr4, Xnr5, and Xnr6) expression, as well as the expression of genes involved in mesodermal (Xmenf, Slug, and Snail) and endodermal (Endodermin and Sox17beta) differentiation.
This gene encodes a member of the SOX (SRY-related HMG-box) family of transcription factors involved in the regulation of embryonic development and in the determination of the cell fate. The encoded protein may act as a transcriptional regulator after forming a protein complex with other proteins. The protein may play a role in tumorigenesis. A similar protein in mice is involved in the regulation of the wingless-type MMTV integration site family (Wnt) pathway.
transcription factor SOX-7
, SRY-box containing gene 7
, SRY (sex determining region Y)-box 7
, SRY (sex determining region Y)-box 7, xSox7 protein
, transcription factor Sox-7