Correlation Engine 2.0
Clear Search sequence regions

  • AKT (1)
  • B Myb (12)
  • b- cell (1)
  • cell cycle (3)
  • E2F2 (6)
  • ERK (1)
  • factors (2)
  • gene (2)
  • human (2)
  • mutual (1)
  • mybl2 protein, human (1)
  • phenotypes (2)
  • protein human (1)
  • protein levels (1)
  • rna (2)
  • Sizes of these terms reflect their relevance to your search.

    B-Myb is an important transcription factor that plays a critical role in gene expression regulation and tumorigenesis. However, its functional implication in colorectal cancer remains elusive. In this study, we found that B-Myb was significantly upregulated at both mRNA and protein levels in colorectal cancer samples compared to non-tumor counterparts. B-Myb overexpression accelerated cell proliferation, cell cycle progression and cell motility in colorectal cancer cells, and promoted tumor growth in orthotopic nude mouse models in vivo. In contrast, B-Myb depletion inhibited these malignant phenotypes. Mechanistic investigations revealed that E2F2 was a novel transcriptional target of B-Myb and is essential to B-Myb-induced malignant phenotypes. Notably, B-Myb and E2F2 exhibited positive expression correlation, and interacted with each other in colorectal cancer cells. In addition to their autoregulatory mechanisms, B-Myb and E2F2 can also directly transactivate each other, thus constituting consolidated reciprocal feed-forward transactivation loops. Moreover, both B-Myb and E2F2 are required for the activation of ERK and AKT signaling pathways in colorectal cancer cells. Taken together, our data clarified a critical role for B-Myb in colorectal cancer and unraveled an exquisite mutual collaboration and reciprocal cross regulation between B-Myb and E2F2 that contribute to the malignant progression of human colorectal cancer. © 2021. The Author(s).


    Xiaoyan Fan, Yitao Wang, Tinghui Jiang, Tao Liu, Yuelei Jin, Kailong Du, Yulong Niu, Chunxue Zhang, Zhongyu Liu, Yunlong Lei, Youquan Bu. B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2. Oncogene. 2021 Sep;40(37):5613-5625

    Expand section icon Mesh Tags

    Expand section icon Substances

    PMID: 34316028

    View Full Text