Table 1.
Lung Diseases | Specific miRNA | Expression Level | Target Site/Host Gene | Findings | References |
---|---|---|---|---|---|
COPD | miR-146a | high | COX-2 | targets 3′ UTR of the Cox2 mRNA and suppresses the expression | 1 |
miR-149-3p | low | TLR-4, MyD88 | reduced expression causes overexpression of TLR-4 and MyD88 | 2 | |
miR-145-5p | high | SMAD3, CFTR, SLC26A9 | involved in Th2 response activation, blocks chloride ion channel | 3, 4 | |
miR-199a-5p | low | Unfolded protein responses | intensification of the UPR | 5 | |
miR-101 and miR-144 | high | MKP-1, TGF-β signaling | induce inflammatory responses | 6 | |
miR-15b | high | SMAD7 | induces TGF-β signaling | 7 | |
Asthma | miR-126 | high | TLRs | activation of inflammatory pathways | 8 |
miR-21 | high | IL-12p35 | modulates IL-12 expression and polarizes Th cells toward Th2 response | 9 | |
miR-155 and miR-146a | high | transcription factor PU.1 and IL-4 | contributes to immediate inflammation and allergic reactions | 10 | |
miR-133a | low | RhoA | excessive bronchial smooth muscle (BSM) contraction | 11 | |
miR-221 and miR-222 | high | p21WAF1 and p27kip1 | involved in mast cell activation and release several growth factors | 12 | |
miR-106a | high | IL-10 | increases pro-inflammatory cytokines release | 13, 14 | |
miR-181 | high | NF-κB | induces increased TCR sensitivity | 15 | |
miR-19a | high | PI3K, JAK-STAT, NF-κB signaling | promotes allergic inflammatory phenotype | 16, 17 | |
Lung cancer | miR-193 | low | KRAS | promotes cellular proliferation, differentiation, and migration | 18 |
miR-17-92 | high | myc | promotes hyper-proliferation of lung epithelial cells | 19 | |
miR-21 | high | PTEN, PDCD4 | promotes growth and invasion in NSCLC | 20 | |
miR-137 | low | SLC22A18 | promotes aggressive tumor progression | 21 | |
miR-451 | low | RAB14 | induces tumor differentiation and shorter survival | 22 | |
miR-16 | low | p27, Bcl-2, Bax, and caspase-3 | induces cell proliferation and apoptosis | 23 | |
miR-218 | low | HMGB1 | leads to aggressive cell proliferation, migration, and invasion | 24 | |
miR-155 | high | Apaf-1 | resistance to therapy and associated with shorter survival | 25 | |
miR-216 | low | eIF4B, ZEB1 | tumor growth, proliferation, metastasis, and chemoresistance | 26 | |
IPF | Let-7d | low | HMGA2 | increases mesenchymal markers (ACTA2, VIM) and decreases epithelial markers (cytokeratin and TJP1) | 27 |
miR-21 | high | SMAD7 | promotes excessive extracellular matrix (ECM) gene transcription | 28 | |
miR-96 | high | FoxO3a | increases PI3K-Akt activity, thereby promoting IPF fibroblasts | 29 | |
miR-326 | low | 3′ UTR of TGF-β | upregulates profibrotic genes | 30 | |
miR-200 | low | TGF-β signaling | induces epithelial-mesenchymal transition and tumor metastasis | 31 | |
CF | miR-126 | low | TOM1 | causes excessive inflammatory response and airway obstruction | 32, 33 |
miR-138 | low | SIN3A | resuscitates the CFTR expression | ||
miR-155 | high | MAPK and PI3K/Akt signaling | activates proinflammatory cytokine IL-8 to attract neutrophils | 34 | |
miR-145 and miR-223 | high | 3′ UTR of CFTR | decrease CFTR expression and cause inflammation | 35 | |
miR-509 and miR-494 | high | NF-κB signaling | repress CFTR expression and induce pro-inflammatory cytokines | 36 | |
miR-93 and miR-31 | low | 3′ UTR of IL-8, IRF-1 | promote increased production of cathepsin S | 37 |
High and low indicate whether the miRNA is elevated or reduced in lung-associated diseases, respectively. CF, cystic fibrosis; COPD, chronic obstructive pulmonary disease; IPF, idiopathic pulmonary fibrosis.