-
Study find that c-Myb is abnormally overexpressed in colorectal cancer (CRC) tissues and correlated with lymph node metastasis. High expression of c-Myb is an independent unfavorable factor affecting patient prognosis. c-Myb promotes the growth and metastasis of CRC cells through epithelial-mesenchymal transition by upregulating c-fos. These findings indicate that c-Myb is a promising prognostic indicator for CRC.
-
MiR-363-3p was significantly highly expressed in osteoporotic samples. Mechanistically, miR-363-3p promotes osteoclastogenesis and inhibits osteogenic differentiation by targeting PTEN and therefore activating PI3K/AKT signaling pathway. MiR-363-3p was activated by its upstream transcription activator MYB
-
We demonstrated that exosomes delivered miR-130a from gastric cancer cells into vascular cells to promote angiogenesis and tumor growth by targeting c-MYB both in vivo and in vitro. miR-130a packaged in exosomes secreted from cancer cells acts as a driver of angiogenesis.
-
Results demonstrated that MYB is aberrantly overexpressed in salivary adenoid cystic carcinoma (SACC) tissues, and promotes SACC cell proliferation and metastasis.
-
Breast adenoid cystic carcinomas probably constitute a convergent phenotype, whereby activation of MYB and MYBL1 and their downstream targets can be driven by the MYB-NFIB fusion gene, MYBL1 rearrangements, MYB amplification, or other yet to be identified mechanisms.
-
Data observe that increasing and decreasing the helical stability of c-Myb over a broad range has a small effect on the binding affinity to KIX domain of CREB binding protein. To reduce the binding affinity by more than 1 kcal/mol, it was necessary to introduce glycine or proline in the middle of the c-Myb helix.
-
In the present study, MYB or MYBL1 locus rearrangement was detected in nearly all adenoid cystic carcinoma cases, and therefore it would be a good diagnostic marker for adenoid cystic carcinoma.
-
Collectively, our data showed that ZFAS1 contributed to the development of AML by sequestering miR-150 from Myb or Sp1, elucidating the central roles of ZFAS1/miR-150/Myb and ZFAS1/miR-150/Sp1 pathways in the tumorigenesis of AML and deepening our understanding on the etiology of leukemia.
-
The presence of the MYB fusion in intermediate-grade and hybrid carcinomas that at least partially exhibit an epithelial-myoepithelial carcinoma phenotype may in fact point to an adenoid cystic carcinoma.
-
The c-Myb gene encodes a transcription factor that regulates cell proliferation, differentiation, and apoptosis through protein-protein interaction and transcriptional regulation of signaling pathways. The protein is frequently overexpressed in human leukemias, breast cancers, and solid tumors suggesting that it is a bona fide oncogene. c-MYB is often overexpressed by chromosomal translocation in human tumors. [review]
-
Low c-myb expression promotes breast cancer lung metastasis.
-
High c-myb expression is associated with In-Stent Restenosis in Peripheral Artery Disease.
-
Data provide evidences supporting the role of Sema5A in melanoma progression and the involvement of Bcl-2, miR-204 and c-Myb in regulating its expression.
-
The data demonstrate that c-Myb plays a critical role in the activation of NK cells and therefore is a therapeutic target for cancer and viral diseases.
-
found no significant differences in the genetic distribution and allelic frequency of MYB and SOX-6 gene polymorphisms
-
Salivary gland ACC cases expressing the MYB-NFIB chimeric gene showed significantly higher blood vessels density compared to non-expressing cases, and suggested that higher VEGF production capability in the former cases may be the cause. The findings also suggested that MYB-NFIB chimeric gene expression may be related to the onset age of ACC.
-
These results indicated that low expression of Mda-7/IL-24 along with high expression of C-myb are predictors for poor prognosis of Burkitt lymphoma patients; this outcome suggests that Mda-7/IL-24 and C-myb might be potential targets for clinical treatment of Burkitt lymphoma.
-
C-Myb expression in the laryngeal squamous cell carcinoma.YB-1 regulates miR-155 expression via c-Myb in the laryngeal squamous cell carcinoma.
-
Data indicate a pioneer factor model in which c-Myb binds to regions of closed chromatin and then recruits histone acetyltransferases. By binding to histones, c-Myb facilitates histone acetylation, acting as a cofactor for p300 at c-Myb binding sites. The resulting H3K27ac leads to chromatin opening and detachment of c-Myb from the acetylated chromatin.
-
Both cases harbored the MYB-NFIB gene fusion as demonstrated by FISH and RNA-sequencing