Downregulation of miR-145 arises from a multifaceted regulatory network: (1) lncRNA sponging by MALAT1 and HOTAIR, which sequester miR-145 in NSCLC cells; (2) promoter hypermethylation at the miR-145 host gene locus (5q32), particularly in TP53-mutant tumors; and (3) transcriptional repression by oncogenic signals such as EGFR-activated ERK, which suppresses miR-145 biogenesis [21,23,24]. Here, HOTAIR is linked to non-small cell lung carcinoma.