Table 2 Pathways of miRNA dysregulation in lung cancer [88]

Genomic abnormalities

Approximately 25% of miRNA genes are placed in chromosomal breakpoints, fragile sites, and areas lacking heterozygosity (LOH) or amplification. miRNAs are susceptible to genomic changes.

In lung cancer, a minimum LOH area of 17p13was nearly (1.9 Mb) equaled with the hsa-miR-22 cluster, and a place of homozygous deletion on 21q11 was near (2.8 Mb) the hsa-let-7c cluster [89].

Epigenetic modifications

DNA methylation and histone modifications could inhibit anti-oncogenes and subscribe to cancer beginning and development.

MiR-9/3, miR-193a, and miR-34b/c were the objectives of epigenetic inhibiting via DNA methylation in lung cancer [90, 91].

Polymorphisms of miRNAs

Single nucleotide polymorphism (SNP) between the miRNA nucleotides

SNP (LCS6) in the 3′-UTR of the KRAS gene, which modified the desire to connect of let-7, was identified to be related to lung tumor danger in low-intensity cigarette smoking [92].

Transcriptional regulation

Pri-miRNA transcription is modulated via transcription agents or genes that are dysregulated in the tumor.

Myc and E2F transcription factor 1 was identified to impact the expression levels of the oncomiR miR-17-92 cluster [93].

Abnormal maturation pathways

Abnormality or impairment in the function of Drosha and Dicer in the procedure of immature pri-miRNAs into a pre-miRNA.

Knockdown of KH-type splicing regulatory protein (KSRP), which improves these RNase III enzymes, could suppress the expression of let-7a and miR-206 and thus impact cell proliferation and differentiation [94].