The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c-Myc expression.

Previous research testifies that c-Myc may promote keloid fibroblast proliferation and collagen accumulation. Ubiquitin-specific peptidase 37 (USP37)-mediated deubiquitination and stabilisation of c-Myc are vital for lung cancer proliferation, while the potential role of USP37 in keloid fibroblasts is not investigated. Elevated USP37, c-Myc, and Collagen I content were detected in keloid tissue with RT-PCR or ELISA assay.

FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c-Myc expression.

C-MYC-mediated keloid fibroblasts proliferation and collagen deposit may contribute to the development of keloids. F-box and leucine-rich repeat protein 6 (FBXL6) is reported to be involved in tumour progression, while the role of FBXL6 in keloid fibroblasts is not deciphered. Normal control skins, hypertrophic scars and keloid tissues were collected and prepared for FBXL6 detection.

Keratinocytes-Derived Reactive Oxygen Species Play an Active Role to Induce Type 2 Inflammation of the Skin: A Pathogenic Role of Reactive Oxygen Species at the Early Phase of Atopic Dermatitis.

Background: Atopic dermatitis (AD) is characterized by chronic, relapsing skin inflammation (eczema) with itchy sensation. Keratinocytes, which are located at the outermost part of our body, are supposed to play important roles at the early phase of type 2 inflammation including AD pathogenesis.

Objective: The purpose of this study was to evaluate whether keratinocytes-derived reactive oxygen species (ROS) could be produced by the allergens or non-allergens, and the keratinocytes-derived ROS could modulate a set of biomarkers for type 2 inflammation of the skin.

CircMYC Regulates Glycolysis and Cell Proliferation in Melanoma.

Circular RNAs (cicRNAs) have been identified to play pivotal roles in several cancer types. However, functions of circRNA in malignant melanoma are poor defined. Our current study demonstrated that human circMYC was obviously upregulated in human melanoma tissue.