Abstract
Basal cell carcinoma (BCC) is the most common skin cancer. While most of the basal cell carcinomas were localized lesion and can be easily managed, the treatment options to the advanced basal cell carcinomas are still remarkably limited. In recent years, proBDNF and its receptor p75NTR have been reported to play important roles in various diseases, including cancers and psychotic disorders. However, the role of p75NTR/proBDNF signaling in basal cell carcinoma remains unclear. Here, we found that the expression level of p75NTR/proBDNF was decreased in basal cell carcinoma patient samples and cell lines. In vitro study showed overexpression of p75NTR/proBDNF could significantly facilitate tumor cell death, including inflammatory-silent apoptosis and lytic inflammatory activated necroptosis. In vivo study showed overexpression of p75NTR/proBDNF dramatically promotes tumor-associated macrophage (M1) and T cell recruitment in a syngeneic mouse model of BCC. These results show a crucial role for p75NTR/proBDNF signaling in basal cell carcinoma immune microenvironment.
Highlights
Basal cell carcinomas (BCCs) are common and costly skin cancer
We found that proBDNF/p75NTR overexpression could modulate BCC immune microenvironment
To investigate the potential roles of proBDNF/p75NTR in BCC progression, the expression levels of proBDNF/p75NTR in BCC and control were evaluated by using western blotting
Summary
Basal cell carcinomas (BCCs) are common and costly skin cancer. The recent data point showed 5.4 million BCCs, and squamous cell carcinomas (SCCs) were diagnosed in 3.3 million Americans and showed a rising tendency [1,2,3]. The established BCC etiologies were environmental changes, and genetic disorders include Gorlin-Goltz syndrome and Xeroderma Pigmentosum [4]. Recurrence is common (10-20% recurrence rate posttreatment for five years) and might lead to a significantly worse prognosis [5]. Some subsets of BCCs, like the advanced basal cell carcinomas (aBCCs), are challenging to treat, and the prognosis is dismal. These facts made the further understanding of BCC pathogenesis became a necessary and urgent topic
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