MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis

Abstract

Limitless cell proliferation, evasion from apoptosis, dedifferentiation, metastatic spread and therapy resistance: all these properties of a cancer cell contribute to its malignant phenotype and affect patient outcome. MYBL2 (alias B-Myb) is a transcription factor of the MYB transcription factor family and a physiological regulator of cell cycle progression, cell survival and cell differentiation. When deregulated in cancer cells, MYBL2 mediates the deregulation of these properties. In fact, MYBL2 is overexpressed and associated with poor patient outcome in numerous cancer entities. MYBL2 and players of its downstream transcriptional network can be used as prognostic and/or predictive biomarkers as well as potential therapeutic targets to offer less toxic and more specific anti-cancer therapies in future. In this review, we summarize current knowledge on the physiological roles of MYBL2 and highlight the impact of its deregulation on cancer initiation and progression.

Expanded huntingtin CAG repeats disrupt the balance between neural progenitor expansion and differentiation in human cerebral organoids

“…Consistent with the enrichment of DEGs for cell cycle genes, E2F and MYB consensus-binding motifs were identified as the top two motifs enriched amongst genes downregulated in IsoHD-81Q organoids ( Figure 4D). The transcription factors (TF) E2F and MYB play a key role in cell cycle control [38,39]. Expression levels of several members of the E2F TF family such as E2F1, E2F3, E2F4 and E2F5 were significantly lower in IsoHD-81Q compared with 30Q organoids ( Figure 4E).…”

Iterative feature selection method to discover predictive variables and interactions for high-dimensional transplant genomic data

“…In addition, mutations in IDH1 is reported to be highly correlated with higher expression of ZIP11, suggesting a possible synergistic interaction between IDH1 and ZIP11 [47]. MYBL2 (rs285206) has an essential role in cell cycle progression, cell survival, and cell differentiation, and is found to be overexpressed in multiple cancer cases [48]. Overexpression of MYBL2 is suggested to have a prognostic value for disease-free survival and cumulative incidence of remission for AML patients [48,49].…”

Common TDP1 Polymorphisms in Relation to Survival among Small Cell Lung Cancer Patients: A Multicenter Study from the International Lung Cancer Consortium

“…MAX could also be either an enhancer (forming heterodimers with MYC, MYC-MAX) or a repressor (forming heterodimers with MAD, MAD-MAX or homodimers, MAX-MAX) (34–36). Overexpression of MYBL2 has been found in several cancer types and associated with poor patient outcomes (review in (37)). Moreover, studies in cell lines suggest that overexpression of MYBL2 is associated with resistance to chemotherapeutic agents (including etoposide) and radiation (38–40).…”