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. Author manuscript; available in PMC: 2018 Aug 15.
Published in final edited form as: Clin Cancer Res. 2017 Apr 7;23(16):4831–4842. doi: 10.1158/1078-0432.CCR-17-0146

Figure 5. Schematic representation of DNA methylation, miR-155-5p, KPC1, and p105 processing into p50 in melanoma.

Figure 5

(A) In primary melanoma, where methylation represses miR-155-5p expression and KPC1 is highly expressed, excess p50–p50 homodimers suppress tumor-promoting p65–p50 heterodimers or modify transcription of NF-κB-target genes with other transcriptional modulators, resulting in suppressive effect on melanoma cell proliferation. (B) Contrarily, metastatic melanoma, which has low DNA methylation / high miR-155-5p and low KPC1 expression, lacks excess p50–p50 homodimers, promoting cell proliferation.