Nude mice study further confirmed an increased tumor growth in Id1-overexpressing cells and a decreased tumor growth in Id1-knockdowned cells. In conclusion, inactivation of Id1 may provide a novel strategy for treatment of lung cancer patients

Id-1 is considered to be a candidate for new therapeutic target and a prognostic factor in non-small cell lung cancer.

The results demonstrate that Id-1B decreases the malignancy of lung and prostate cancer cells and counteracts the protumorigenic role of the classical form of Id-1.

Data indicate that grap2 and cyclin D1 interacting protein (GCIP) and inhibitor of of DNA binding/differentiation 1 (Id1) are inversely expressed in non-small cell lung cancer (NSCLC) cell lines and specimens.

ID1 expression was positively related to drug resistance of EGFR-TKI in non-small cell lung cancer.

Id1 enables lung cancer liver colonization by activating an epithelial mesenchymal transformation program in tumor cells and establishing the pre-metastatic niche.

Findings highlight the prognostic significance of the transcriptional regulator Id1 in KRAS-mutant lung adenocarcinoma and provide mechanistic insight into how it controls tumor growth and metastasis.

ZEB1-AS1 can promote cell proliferation and migration of non-small cell lung carcinoma cells by silencing ID1 expression.

ID1 overexpression increases gefitinib sensitivity in non-small cell lung cancer by activating RIP3/MLKL-dependent necroptosis.

Id1 enables both Lewis lung carcinoma cells and the host microenvironment for an effective liver colonization.