Therapeutic Use of MicroRNAs in Lung Cancer

Table 1

Principal miRNAs involved in lung carcinogenesis.

miRNAs	Expression in lung cancer	Cellular processes affected and targets	Reference
Let-7 family	Decreased	(i) Cell proliferation (KRAS, MYC, and HMGA2)	[28–30]
		(ii) miRNA maturation Dicer mediated	[31]
		(iii) Cell-cycle regulation (CDC25A, CDK6, and cyclin D2)	[32]
mir-34 family	Decreased	(i) Transcriptionally activated by p53	[40]
		(ii) TRAIL-induced cell death and cell proliferation (BCL-2, MET, and PDGFR-α/β)	[41–43]
mir-21	Increased	(i) Apoptosis, cellular proliferation, and migration (TPM1, PDCD4, and PTEN)	[50–53]
		(ii) TKI-treatment resistance	[54]
mir-17/92a cluster	Increased	(i) Transcriptionally regulated by c-MYC	[60]
		(ii) Cellular proliferation and cancer development (PTEN, HIF-1a CL2L11, CDKNA, and TSP-1)	[57, 61–63]
mir-15a/16 cluster	Decreased	Cell cycle regulation (cyclin D1, D2 and E1)	[66, 67]
mir-200 family	Decreased	Promotion of EMT and metastasization; (ZEB transcription factors,CDH-1, and vimentin)	[68–73]
miRNA-29 family	Decreased	Epigenetic regulation of gene expression; (DNMT-3A and DNMT-3B)	[74]
mir-221/mir-222	Increased	(i) TRAIL resistance and cellular migration (PTEN and TIMP3)	[75, 76]
		(ii) Transcriptionally regulated by EGFR and MET and gefitinib resistance (BIM and APAF1)	[77]
mir-548	Decreased	Tumor cell growth; (CCND, ERBB2, DMNT3A, and DNMT3B)	[78]