B-Myb is a transcription factor that is overexpressed and plays an oncogenic role in several types of human cancers. However, its potential implication in lung cancer remains elusive. In the present study, we have for the first time investigated the expression profile of B-Myb and its functional impact in lung cancer. Expression analysis by quantificational real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry demonstrated that B-Myb expression is aberrantly overexpressed in non-small cell lung cancer (NSCLC), and positively correlated with pathologic grade and clinical stage of NSCLC. A gain-of-function study revealed that overexpression of B-Myb significantly increases lung cancer cell growth, colony formation, migration, and invasion. Conversely, a loss-of-function study showed that knockdown of B-Myb decreases cell growth, migration, and invasion. B-Myb overexpression also promoted tumor growth in vivo in a NSCLC xenograft nude mouse model. A molecular mechanistic study by RNA-sequencing (RNA-seq) analysis showed that B-Myb overexpression causes up-regulation of various downstream genes (e.g., COL11A1, COL6A1, FN1, MMP2, NID1, FLT4, INSR, and CCNA1) and activation of multiple critical pathways (e.g., extracellular signal-regulated kinases (ERK) and phosphorylated-protein kinase B (Akt) signaling pathways) involved in cell proliferation, tumorigenesis, and metastasis. Collectively, our results indicate a tumor-promoting role for B-Myb in NSCLC and thus imply its potential as a target for the diagnosis and/or treatment of NSCLC.

B‑Myb is a critical transcription factor in regulating cell cycle. Dysregulated expression of B‑Myb promotes tumor formation and development. B‑Myb is a proto‑oncogene ubiquitously expressed in proliferating cells, which maintains normal cell cycle progression. It participates in cell apoptosis, tumorigenesis and aging. In addition, B‑Myb is overexpressed in several malignant tumors, including breast cancer, lung cancer and hepatocellular carcinoma, and is associated with tumor development. B‑Myb expression is also associated with the prognosis of patients with malignant tumors. Both microRNAs and E2F family of transcription factors (E2Fs) contribute to the function of B‑Myb. The present review highlights the association between B‑Myb and malignant tumors, and offers a theoretical reference for the diagnosis and treatment of malignant tumors.