Circ_0081054 facilitates melanoma development via sponging miR-637 and regulating RAB9A.

Background: Accumulating evidence announces that aberrantly expressed circRNAs were closely related to the development of human cancers. However, the role and mechanism of multiple circRNAs remain unclear. Our work aimed to disclose the functional role and mechanism of circ_0081054 in melanoma.

Ubiquitin-specific protease 34 in macrophages limits CD8 T cell-mediated onset of vitiligo in mice.

As an autoimmune disorder, vitiligo is characterized by depigmented skin macules. CD8T cells and macrophages enrichment promote the onset of vitiligo, while the role of macrophages to CD8T is not well deciphered. To develop a mouse model of vitiligo with prominent epidermal depigmentation, Krt14-Kitl* transgenic mice containing an elevated number of melanocytes in the epidermis with membrane-bound Kit ligand (Kitl*) were adoptively transferred with premelanosome protein (PMEL) CD8 T cells.

The circular RNA circCRIM1 inhibits osteosarcoma progression through sponging miR-513.

Numerous studies have suggested that the abnormal expression of circular RNAs plays an essential role in the pathological progression of numerous tumors. Nonetheless, the functions and underlying mechanisms of the circular RNA circCRIM1 in osteosarcoma (OS) are still not fully understood. In this study, 47 classes of OS tissues and adjoining normal tissues were obtained from patients.

Depletion of circRNA circ_CDK14 inhibits osteosarcoma progression by regulating the miR-520a-3p/GAB1 axis.

Osteosarcoma (OS) is a lethal bone malignancy. Circular RNAs (circRNAs) have emerged as important regulators of OS development. CircRNA cyclin dependent kinase 14 (circ_CDK14) was reported to be a potential oncogene in OS.

CCL17-CCR4 axis contributes to the onset of vitiligo in mice.

Background: Destruction of melanocytes mediated by autoimmunity is currently believed as the main cause of vitiligo. This article aims to identify the role of CC chemokine ligand 17 (CCL17)-CC chemokine receptor 4 (CCR4) axis in vitiligo and provide new possibilities for the clinical treatment of vitiligo.

Methods: A total of 30 patients with vitiligo from Affiliated Huaian No.

CircRNA circ_0067772 aggravates the malignant progression of cutaneous squamous cell carcinoma by regulating miR-1238-3p/FOXG1 axis.

Background: Cutaneous squamous cell carcinoma (CSCC) is a severe malignancy derived from skin. Dysregulated circular RNAs (circRNAs) might play vital roles in tumor development.

Objective: Here, we aimed to explore the function of a novel circRNA circ_0067772 in CSCC.

A20 deficiency in myeloid cells deteriorates the onset of vitiligo in mice.

Melanocyte-specific CD8 T cells enrichment correlates with the severity of vitiligo, and the role of A20 derived from myeloid cells in the enrichment of pathogenic T cells is unknown. Premelanosome (PMEL)-specific transgenic CD8 T cells were adoptive transferred into Krt14-Kitl* mice to construct the vitiligo model, which was further mated with A20 mice and IKK2 mice. Bone marrow cells were stimulated with 30% L929 cell-conditioned medium, Fc-human tumor necrosis factor, and lipopolysaccharides to induce bone marrow-derived macrophages (BMDMs).

Juglanin administration protects skin against UVB‑induced injury by reducing Nrf2‑dependent ROS generation.

Extensive solar ultraviolet B (UVB) exposure of the skin results in inflammation and oxidative stress, which may contribute to skin cancer. Natural products have attracted attention for their role in the effective treatment of cutaneous neoplasia. Juglanin is purified from the crude extract of Polygonum aviculare, exhibiting anti‑oxidant, anti‑inflammatory and anti‑cancer activities.

Hyperoside exerts potent anticancer activity in skin cancer.

Quercetin-3-O-β-D-galactopyranoside, is a hyperoside flavonol glycoside with anti-cancer, anti-inflammatory, and anti-oxidant activities that is derived from Hypericum and Crataegus plants. To this end, we examined the effect of this hyperoside in skin cancer cells lines and in DMBA/TPA induced skin tumors . treatment of cancer cells with hyperoside significantly inhibited phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/p38 MAPK axis, concomitantly activated the 5'AMP-activated protein kinase (AMPK) signaling, inhibited proliferation, and induced apoptosis and autophagy.

Liquiritin suppresses UVB‑induced skin injury through prevention of inflammation, oxidative stress and apoptosis through the TLR4/MyD88/NF‑κB and MAPK/caspase signaling pathways.

Solar ultraviolet B (UVB) radiation is known to trigger inflammation, oxidative stress and apoptotic responses through various signaling pathways, which eventually lead to skin cancer. The present study investigated whether liquiritin suppresses UVB‑induced skin injury in vivo and in vitro using SKH‑1 hairless mice and HACAT cells, respectively. The animals were exposed to UVB irradiation (180 mJ/cm2) for 20 min, followed by liquiritin treatment.

Salidroside prevents skin carcinogenesis induced by DMBA/TPA in a mouse model through suppression of inflammation and promotion of apoptosis.

Salidroside (SR) is a main component of Rhodiola rosea L. and exhibits a variety of pharmacologic properties. The present study was carried out to explore the potential effect of SR against skin cancer induced by 7,12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13‑acetate (TPA) in female Institute for Cancer Research (ICR) mice and to reveal the underlying molecular targets regulated by SR.