Our results suggest that, in addition to the RB1 gene, abnormalities of other tumor-suppressor genes on chromosome 13q are involved in the development of human NSCLCs.
Low levels of p27 in association with deregulated p53-pRb protein status enhance tumor proliferation and chromosomal instability in non-small cell lung carcinomas.
For LCNEC tumors, the unsupervised gene expression analysis suggested two different transcriptional patterns corresponding to a proposed genetic division of LCNEC tumors into SCLC-like and NSCLC-like cancer on the basis of TP53 and retinoblastoma 1 gene (RB1) alteration patterns.
This study, for the first time, elucidates nicotine-miR-99b/miR-192-FGFR3/RB1 regulatory network that nicotine promotes NSCLC cell proliferation and EMT by downregulating miR-99b and miR-192, and upregulating their targets FGFR3 and RB1.