548P - B-Myb acts as a mentor instant promoter in non-small cell lung cancer by modifying the PD-1/PD-L1 axis

Background

Lung cancer is the malignant tumor with the highest incidence rate and mortality in the world. The main types of lung cancer are nonsmall cell lung cancer (NSCLC) and small cell lung cancer (SCLC). With targeted therapy and immunotherapy emerging, treating NSCLC has made a great progress. However, the molecular mechanisms underlying progression of NSCLC remain elusive.

Methods

Completing gain- and loss-of-function experiments to view whether B-Myb regulates the function of lung cancer cells by targeting IGFBP3 in lung cancer cell lines H1299 and A549, respectively. Mechanistically, Using a stable strain of B-Myb lung cancer to build the animal model and collecting mouse blood to lymphocyte subgroup analysis by flow cytometry. Analyzing metabolic products of lung cancer by metabolomics.

Results

B-Myb increased in lung cancer tissues and cells notably, its expression interrelated with clinical stage and poor prognosis of patients with NSCLC. B-Myb may affect the proliferation, invasion, and migration of NSCLC by regulating IGFBP3. Importantly, overexpressing of B-Myb in NSCLC affects the expression of immune checkpoint PD-1/PD-L1 and lung cancer cell metabolism.

Conclusions

Our findings reveal that B-Myb may interact with IGFBP3 to promote the occurrence and development of NSCLC and affect immune checkpoints PD-1/PD-L1 expressing. B-Myb may become a potential new target for the diagnosis and treatment of NSCLC.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Chongqing Municipal Education Commission.

Disclosure

All authors have declared no conflicts of interest.