Posted: Monday, March 7, 2022
According to Jolanta Jura, PhD, of Jagiellonian University, Krakow, Poland, and colleagues, the level of the monocyte chemotactic protein 1–induced protein 1 (MCPIP1) tends to vary in the skin depending on the type of skin lesion. This variation may range from high in benign lesions such as actinic keratoses to very low in advanced stages of malignant transformation such as squamous cell carcinoma. The findings of this preclinical study were published in the Journal of Experimental & Clinical Cancer Research.
“Our studies in mice with keratinocyte-specific knockout of the gene encoding monocyte chemotactic protein 1 and subjected to chemical carcinogenesis showed for the first time that RNase MCPIP1 participated in tumor initiation and progression,” said the authors.
The study analyzed the distribution of MCPIP1 in skin biopsies of patients with actinic keratoses and squamous cell carcinoma. The investigators created a mouse model to chemically induce carcinogenesis to explore the mechanisms by which this protein may modulate tumorigenesis in vivo.
Skin expression of MCPIP1 changed during the transformation of precancerous lesions into cutaneous squamous cell carcinoma. Immunoreactivity of this protein was high in the thickened area of the actinic keratoses epidermis but was predominantly restricted to keratin pearls in fully developed squamous cell carcinoma lesions. Accelerated development of chemically induced skin tumors was observed in mice with loss of epidermal MCPIP1. Papillomas that developed in the skin of mice with the loss of epidermal MCPIP1 were larger and characterized by elevated expression of markers typical of keratinocyte proliferation and tumor angiogenesis, according to the authors’ findings. Moreover, their results demonstrated that in keratinocytes, RNase MCPIP1 is essential for the negative regulation of genes encoding squamous cell carcinoma antigens and matrix metallopeptidase 9.
Disclosure: For full disclosures of the study authors, visit jeccr.biomedcentral.com.