Abstract
Chondroitin polymerizing factor (CHPF) is an important member of glycosyltransferases involved in the biosynthesis of chondroitin sulfate (CS). However, the relationship between CHPF and malignant melanoma (MM) is still unknown. In this study, it was demonstrated that CHPF was up-regulated in MM tissues compared with the adjacent normal skin tissues and its high expression was correlated with more advanced T stage. Further investigations indicated that the over-expression/knockdown of CHPF could promote/inhibit proliferation, colony formation and migration of MM cells, while inhibiting/promoting cell apoptosis. Moreover, knockdown of CHPF could also suppress tumorigenicity of MM cells in vivo. RNA-sequencing followed by Ingenuity pathway analysis (IPA) was performed for exploring downstream of CHPF and identified CDK1 as the potential target. Furthermore, our study revealed that knockdown of CDK1 could inhibit development of MM in vitro, and alleviate the CHPF over-expression induced promotion of MM. In conclusion, our study showed, as the first time, CHPF as a tumor promotor for MM, whose function was carried out probably through the regulation of CDK1.
Highlights
Malignant melanoma (MM) is a highly malignant neoplasm originating from melanocytes in the basal layer of epidermis, which is predominant in the skin or mucosa adjacent to the skin[1]
In order to investigate the role of Chondroitin polymerizing factor (CHPF), exploring the molecular mechanism of MM, the expression level of CHPF was detected by immunohistochemistry (IHC) analysis of a human MM tissue microarray (TMA)
Mice were sacrificed through injection of pentobarbital sodium, and the tumors were removed for taking photos and weighting
Summary
Malignant melanoma (MM) is a highly malignant neoplasm originating from melanocytes in the basal layer of epidermis, which is predominant in the skin or mucosa adjacent to the skin[1]. Because MM has no specific markers for early clinical diagnostic and is characterized by rapid progression, satellite foci, local lymph node metastasis and distant metastasis could appear soon after the onset of melanoma, causing the approximate 10% 5-year survival rate for patients with advanced MM2. It has been well documented that the overexpression of cancer-promoting genes plays an important role in the development and progression of human cancers[8]. The exploration of cancer-promoting genes and the underlying mechanism of their promotion effect on MM could deepen the understanding of the molecular mechanism of MM, and have important significance for clinical diagnosis and treatment.
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