Psoriasis, a common skin inflammatory disorder, is characterized by the aberrant growth and differentiation of keratinocytes. Ar-Turmerone, a main bioactive ingredient of Curcuma longa , has been found to alleviate skin inflammation in psoriasis-like mice. However, the effects and underlying mechanism of ar-turmerone on keratinocytes remain unknown. The effects of ar-turmerone alone or combined with recombinant human sonic hedgehog (rhShh) on cell proliferation, apoptosis, and inflammatory cytokine secretion were explored by MTT, flow cytometry analysis, and ELISA, respectively. The mRNA and protein levels of Shh, glioblastoma-1 (Gli1), and smoothened (SMO) were determined by RT-qPCR and western blot analysis, respectively. Results disclosed that ar-turmerone dose-dependently suppressed proliferation, facilitated apoptosis, and reduced TNF-α-mediated production of interleukin (IL)–1β, IL-6, and IL-8 in HaCaT cells. Ar-turmerone blocked Hedgehog pathway in HaCaT cells, as evidenced by the reduced expression of Shh, Gli1, and SMO. Moreover, activation of the Hedgehog pathway by rhShh abolished the effects of ar-turmerone on the proliferation, apoptosis, and TNF-α-mediated inflammatory cytokine expression in HaCaT cells. In conclusion, ar-turmerone suppressed cell proliferative ability and attenuated inflammatory cytokine expression by inactivating Hedgehog pathway in HaCaT cells, contributing to better understanding the potential anti-psoriasis effects of ar-turmerone on psoriasis.

Aristaless-like homeobox1 (ALX1), a member of the ALX family, is capable of mediating survival and development of mesenchyme-derived elements in vertebrates and its mutation will prevent the fusion of frontonasal and maxillary elements. Recently, ALX1 has been reported to be associated with cancer progression. However, the specific roles of ALX1 in melanoma remain unclear. In this study, we investigated the expression pattern and biological functions of ALX1 in melanoma. We found that ALX1 was highly expressed in melanoma tissues and cell lines. Knockdown of ALX1 suppressed the proliferation and invasion of melanoma cells. Furthermore, we showed that ALX1 knockdown reversed the epithelial-mesenchymal transition (EMT) process in melanoma cells, which might be attributed to inactivation of the Wnt/β-catenin pathway. Taken together, this study provided a new insight into the role of ALX1 as a therapeutic target for melanoma treatment.