Table 2.
List of lncRNAs whose expression has been up-regulated in the psoriasis.
| LncRNA | Numbers of clinical samples | Source | Targets/Regulators | Signaling Pathways | Function and comments | Reference |
|---|---|---|---|---|---|---|
| PRINS | 6 mm punch biopsies were taken from non-lesional and lesional (n = 4, each) skin areas of patients with psoriasis. Skin biopsies obtained from healthy individuals (n = 7) undergoing plastic surgery were used as control samples. | Keratinocytes | G1P3 | Apoptosis | G1P3 suppresses spontaneous keratinocyte apoptosis and its high expression in psoriatic skin participates to increased cell production rate and epidermal thickness in psoriasis. Overexpression of PRINS in Psoriatic non-lesional epidermis may act as a trigger factor to induce the expression of the anti-apoptotic G1P3 protein that participates to the maintenance of the keratinocyte hyperproliferation in the evolving psoriatic lesions. | [16] |
| MIR31HG | Punch biopsies (4 mm) were taken from lesional skin areas of 10 patients with psoriasis. Normal skin specimens were taken from healthy individuals undergoing plastic surgery. | HaCaT keratinocytes/Lesional skin tissues | IL-17A, IL-22, TNF-α or IL-1α target NF-κB signaling. MIR31HG expression is dependent on NF-κB activation. | NF-κB signaling | siRNA-mediated MIR31HG depletion induced cell cycle arrest in the G2/M phase. MIR31HG expression depends on NF-κB activation. | [17] |
| RP6‐65G23.1 | HaCaT cell, a human skin epithelial cell line, and Human Normal Primary Epidermal Keratinocytes (HEKn) were used. M5, a cocktail of cytokines, was used to induce psoriatic inflammation like condition in HaCaT cells and primary keratinocytes. | HaCaT and HEKn cell lines | p21, p27, Bcl‐xl and Bcl2 | P-ERK1/2/p‐AKT signaling pathway | Knockdown of RP6‐65G23.1 resulted in defects of growth and increased rates of apoptosis in HaCaT cells. | [18] |
| MSX2P1 | 10 cases of psoriatic lesions and 10 cases of normal skin tissues were collected. | Keratinocytes, HaCaT and HNEK cells | miR-6731-5p and S100A7 | MSX2P1 acts as an endogenous sponge directly binding to miR-6731-5p and thus, resulting in elevated levels of S100A7 and other proinflammatory cytokines, by suppressing the expression of miR-6731-5p and inducing apoptosis in IL-22-stimulated keratinocytes. | [19] | |
| SLC6A14-1:1 | 15 patients with psoriasis and 15 healthy controls were recruited. | Skin samples | Differentiation and function of Treg cells, NF-κΒ, mTOR, MAPK and JAK-STAT signaling pathway and the release of cytokines and chemokines | The mentioned lncRNAs may be used as potential biomarkers and therapeutic targets for the treatment of psoriasis. | [12] | |
| NR_003062 | ||||||
| SERPINB3-4:1 | ||||||
| NONHSAT006518 | ||||||
| IGFL3-6:1 | ||||||
| ENST00000472053 | ||||||
| NONHSAT006509 | ||||||
| NR_030617 | ||||||
| RAPGEF2-3:1 | ||||||
| RPP40-3:3 |