Pan-cancer analysis indicates that MYBL2 is associated with the prognosis and immunotherapy of multiple cancers as an oncogene

Cell Cycle. 2021 Nov;20(21):2291-2308. doi: 10.1080/15384101.2021.1982494. Epub 2021 Sep 29.

Abstract

MYBL2 has been demonstrated to be an oncogene in some cancers, but there is no pan-cancer analysis at the macro level. We used multiple online or offline bioinformatic tools to examine the effects of MYBL2 in human cancers. We first identified that MYBL2 was highly expressed and related to the stage and grade of most cancers. The results of survival analysis from two databases showed that high MYBL2 expression was positively correlated with a poor prognosis for most cancer patients. We observed a significant difference in the promoter methylation level of MYBL2 in cancers such as colon adenocarcinoma and liver hepatocellular carcinoma versus normal controls. We found that MYBL2 can affect the tumor immune microenvironment by influencing the immune infiltration level and expression level of CD4+ T cells, CD8+ T cells, cancer-associated fibroblasts (CAFs) and immune checkpoint-associated cells. Functional enrichment analysis of MYBL2 identified that MYBL2 can play a crucial role in cancers by regulating spliceosomes, DNA replication and the cell cycle. Moreover, we verified the function of MYBL2 in three cancer cells of glioma, breast cancers and liver cancers, and the results showed that MYBL2 can regulate the cell cycle and proliferation ability of cancers.

Keywords: MYBL2; immune infiltration; methylation; pan-cancer; prognosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / immunology
  • CD8-Positive T-Lymphocytes* / immunology
  • Carcinoma, Hepatocellular* / immunology
  • Carcinoma, Hepatocellular* / therapy
  • Cell Cycle Proteins / metabolism
  • Humans
  • Immunotherapy
  • Liver Neoplasms* / immunology
  • Liver Neoplasms* / therapy
  • Oncogenes
  • Trans-Activators* / immunology
  • Tumor Microenvironment / genetics

Substances

  • Biomarkers, Tumor
  • Cell Cycle Proteins
  • MYBL2 protein, human
  • Trans-Activators

Grants and funding

This work was supported by the National Natural Science Foundation of China (grant nos. 81172405 and 81572490), the Tianjin Science and Technology Committee (grant no. 18JCZDJC98600) and the Science and Technology fund of Tianjin Binhai New Area Health and Family Planning Commission (grant no. 2018BWKZ002).