Nuclear YB-1 expression might be essential for the malignant phenotype in lung cancer patients.

Loss of p53-related suppression of lung resistance-related protein through Y-box binding protein 1 may be the reason for LRP expression increase, and, therefore, chemotherapy resistance in tumor cells.

Nuclear YB-1 localization following high LRP and EGFR expression is associated with non-small-cell lung cancer.

Aberrant expression of both cyclin D1 and CDC6 by YB-1 over-expression may collaboratively participate in lung carcinogenesis.

The long noncoding RNA CAR intergenic 10 bound and stabilized transcription factor Y-box-binding protein 1 (YB-1), leading to up-regulation of the epidermal growth factor receptor (EGFR) and proliferation of lung cancer cells.

Inhibition of YBX1 suppressed lung cancer growth partly via the CDC25a pathway and high expression of YBX1/CDC25a predicts poor prognosis in human lung adenocarcinoma.

YB-1 promoted lung adenocarcinoma growth and progression in vitro and in vivo through directly binding to the MACC1 promoter and enhancing MACC1/c-Met pathway.

Analysis of 918 lung cancer and normal lung tissues and lung cancer cell lines revealed that MIR22HG was significantly downregulated in lung cancer; this decreased expression was associated with poor patient survival. MIR22HG bound and stabilized the YBX1 protein. Silencing of MIR22HG triggered both cell survival and cell death signaling through dysregulation of the oncogenes YBX1, MET, and p21.

LINC00312 induced migration, invasion and VM of lung cancer cells by direct binding to the transcription factor Y-Box Binding Protein 1 (YBX1).

Long non-coding RNA linc00665 interacts with YB-1 and promotes angiogenesis in lung adenocarcinoma.