Intricate crosstalk between MYB and noncoding RNAs in cancer.
Dingyu HuWenjun ShaoLi LiuYanyan WangShunling YuanZhaoping LiuJing LiuJi ZhangPublished in: Cancer cell international (2021)
MYB is often overexpressed in malignant tumors and plays a carcinogenic role in the initiation and development of cancer. Deletion of the MYB regulatory C-terminal domain may be a driving mutation leading to tumorigenesis, therefore, different tumor mechanisms produce similar MYB proteins. As MYB is a transcription factor, priority has been given to identifying the genes that it regulates. All previous attention has been focused on protein-coding genes. However, an increasing number of studies have suggested that MYB can affect the complexity of cancer progression by regulating tumor-associated noncoding RNAs (ncRNAs), such as microRNAs, long-non-coding RNAs and circular RNAs. ncRNAs can regulate the expression of numerous downstream genes at the transcription, RNA processing and translation levels, thereby having various biological functions. Additionally, ncRNAs play important roles in regulating MYB expression. This review focuses on the intricate crosstalk between oncogenic MYB and ncRNAs, which play a pivotal role in tumorigenesis, including proliferation, apoptosis, angiogenesis, metastasis, senescence and drug resistance. In addition, we discuss therapeutic strategies for crosstalk between MYB and ncRNAs to prevent the occurrence and development of cancer.
Keyphrases
- transcription factor
- genome wide identification
- papillary thyroid
- dna binding
- poor prognosis
- long non coding rna
- squamous cell
- genome wide
- endothelial cells
- lymph node metastasis
- squamous cell carcinoma
- binding protein
- signaling pathway
- risk assessment
- dna damage
- working memory
- oxidative stress
- dna methylation
- stress induced
- cell proliferation
- childhood cancer
- amino acid