Expression of cyclin D1 and p16 in psoriasis before and after phototherapy

Abstract

Cyclin D1 upregulation and p16 downregulation may play a role in the pathogenesis of psoriasis. Normalization of the levels of both parameters may be a mechanism by which phototherapy induces remission in psoriasis.

Wnt/β-Catenin and Wnt5a/Ca2+ Pathways Regulate Proliferation and Apoptosis of Keratinocytes in Psoriasis Lesions

“…Indeed, the results of the present study support this, as transfection of keratinocytes with Wnt5a siRNA suppressed cell proliferation and induced apoptosis. Wnt5a knockdown downregulated the expression of PCNA and MKI67 , proliferation markers that can be used to assess epidermal hyperproliferation in psoriasis and malignancy potential for in cutaneous lesions [19], as well as cyclin D1, which is a key regulator of cell cycle progression in psoriasis lesions [20]. These results are in contrast to those reported by Gudjonsson et al [9], who found that exogenous Wnt5a suppressed the growth of keratinocytes.…”

Melanoma and other malignant skin cancers in psoriatic patients treated with phototherapy. Role of the p16 protein in psoriasis

“…Abou et al studied the effect of phototherapy on the p16 expression and found that significantly less protein in psoriatic lesions were observed before phototherapy than in controls. Moreover, they confirmed the stimulating effect of phototherapy on the synthesis of the p16 in the skin [24]. In contrast, Elias et al showed elevated levels of the p16 protein in psoriatic plaque [21].…”

“…In the light of recent studies, a decreased p16 level could be highly disadvantageous in psoriasis. A low level of p16 may contribute to epidermal proliferation and be involved in the pathogenesis of psoriasis [22,24]. Moreover, it seems that the p16 plays an important role in cell defense against mutagenic agents and could be responsible for the delayed apoptosis and the relative resistance to malignant transformation [12,25].…”

“…According to Abou et al, the altered expression of cell-cycle regulatory genes, including the p16, may play a significant role in the pathogenesis of hyperproliferative diseases. The detected decreased level of the p16 indicates a shift of balance toward proliferative rather than senescent processes, which could have an impact on the etiopathogenesis of psoriasis [24].…”

The classical photoactivated drug 8-methoxypsoralen and related compounds are effective without UV light irradiation against glioma cells

“…most probable explanation for this apparent paradox is that the drug can slow down the cell division process by interfering with cell cycle controllers. In fact, it has been demonstrated that, after PUVA therapy, there are changes in cell cycle controlling proteins levels in the patients (Abou El-Ela et al, 2010). The detailed mechanism of action of 8-MOP remains under investigation, but if this hypothesis is confirmed it could prevent side effects common in many antitumor drugs (Terada et al, 2015).…”