Table 4 miR-630 in non-cancerous diseases (ED endothelial dysfunction; NEF normal endothelial function; OB obese)
From: The importance of miRNA-630 in human diseases with an especial focus on cancers
Type of disease | Expression pattern | Samples | Cell lines | Downstream targets | Related molecules and pathways | Function | Refs. |
|---|---|---|---|---|---|---|---|
AIDS | Up | 27 HIV-1 positive women, 9 HIV-1 negative women | – | BCL2, BCL2L2, BCL2L11, and YAP1 | – | miR-630 could be considered as a distinguishing biomarker between HIV1-infected mother milk and non-HIV1-infected mother milk | [50] |
Upper in chronic progressors than others | 13 uninfected controls, 12 chronic progressors and 12 long-term nonprogressors (GEO dataset) | – | PELI1, LAPTM5, EXO1, ZNF131, TMED7 | Enzyme linked receptor protein and receptor quanylyl cyclase signaling pathways | miR-630 could be considered as a putative biomarker for AIDS progression | [51] | |
IgA nephropathy (IgAN) | Down | 27 tonsil tissues from IgAN patients and 20 tonsil tissues from patients with chronic tonsillitis | Tonsil mononuclear cell (TMC) | TLR4, IgA1 | NF-kB signaling pathway | Over-expression of miR-630 caused TLR4 and IgA1 attenuation while glycosylation content of IgA1 was enhanced | [52] |
Obstructive sleep apnea (OSA) | Down in ED | 128 children: OBNEF (n = 23), OBED (n = 20), OSANEF (n = 34), OSAED (n = 25), and Control (n = 26)/mice | Microvascular endothelial cells | 416 different genes | 10 various pathways as tight junction signaling pathways, NRF2-mediated oxidative stress responses and AMP kinase | miR-360 could be postulated as a risk factor of cardiovascular disease in OSA and obesity in children | [54] |
Age-related nuclear cataract | Up | 45 lens epithelium samples from cataract patients | HLE-B3 | WEE2, MAP3K2, MAP4K3, STK39, DEFB132, MAPK14, ANKRD6, RAD1, ATG12, SGTB, MAP3K1, YES1, RB1CC1, BCL2L2, EDNRB, WEE1, FER, PAK7, DCLRE1C, UBXN2A, RAD18, PARP3, SLK, ATG2B, TMX3, BTBD3, TMX1, GPR37, CDC7, PPP2CA, IRAK3, TP63, RHD, FRK, CXCL13, POLR2D, GPX8, ITPR1, TLR4, SLK, UBE2N, SRPK2, CUL4B, TMX4, NBEAL1, CD226, CCL11, PIK3CA, DDB1, NLK | – | H2O2 treatment could overexpress miR-630 and correlated with nuclear opacity and progression of age-related nuclear cataract | [53] |
Cataract | Up | Lens capsules from 25 cataract patients and 25 normal controls | SRA01/04 | E2F3, Bax, cleaved caspase 3, Bcl-2, N-cadherin, vimentin, and a-SMA, E-cadherin | Axon guidance pathway | miR-630 in partnership with miR-378a-5p and by E2F3 targeting inhibited cell growth and EMT but induced cell death | [55] |
Vitiligo | Down | Peripheral blood of 5 vitiligo patients and 5 non-vitiligo cases | – | – | – | miR-630 was identified as a differential expressed miRNA in vitiligo | [56] |
Heterotopic ossification (HO) | Down | Sample of ectopic bone and serum from 146 HO cases, serums sample from 292 patients without HO after taking arthrolysis (control 1), and 292 patients with fracture healing (control 2)/mice | HD-MVEC, and 293T | Slug, osteocalcin, osteopontin and Runx2, VE-cadherin, occluding, N-cadherin, and vimentin | – | Suppression of endothelial-mesenchymal transition by miR-630 via targeting slug could be involved in the formation of ectopic bone in HO | [57] |