RBAK is upregulated in non-small cell lung cancer and promotes cell migration and invasion.

Non-small cell lung cancer (NSCLC) is a leading cause of cancer-associated mortality worldwide, NCSCLC includes lung adenocarcinoma and lung squamous cell carcinoma. Tumor metastasis is the major cause of mortality of patients with NSCLC. However, the mechanisms underlying NSCLC metastasis remain largely elusive. In present study, the authors focused on exploring the roles of RBAK in NSCLC. The present study demonstrated that RB-associated KRAB zinc finger (RBAK) was upregulated in NSCLC compared with non-tumorous tissues by analyzing Gene Expression Omnibus (GEO) datasets and The Cancer Genome Atlas (TCGA) dataset. High expression of RBAK was associated with poor disease-free survival of patients with NSCLC by analyzing TCGA dataset. Furthermore, an RBAK-mediated protein-protein interaction network was constructed to reveal the potential underlying mechanisms by which RBAK drives NSCLC progression. The authors found that RBAK was involved in regulating a number of transcription factors, including androgen receptor, forkhead box A1, tumor protein 53, and E2F transcription factor 1, 2 and 4, suggesting that RBAK may have a role in regulating gene transcription. GO and KEGG enrichment analyses of the genes co-expressed with RBAK revealed that RBAK is involved in regulating a number of biological functions, including the Wnt signaling pathway, mRNA splicing, protein polyubiquitination, cell-cell adhesion and focal adhesion. Transwell and wound healing assays demonstrated that knockdown of RBAK suppressed NSCLC cell migration and invasion. The present study enhances the current understanding of the important roles of RBAK in NSCLC metastasis and may provide useful information for the development of novel treatment approaches.