Abstract
C2ORF40 encodes a secreted protein which is cleaved to generate soluble peptides by proteolytic processing and this process is believed to be necessary for C2ORF40 to exert cell type specific biological activity. Here, we reported a short mimic peptide of human C2ORF40 acts potential therapeutic efficacy in human cancer cells in vitro and in vivo. We synthesized a short peptide of human C2ORF40, named C2ORF40 mimic peptide fragment and assessed its biological function on cancer cell growth, migration and tumorigenesis. Cell growth assay showed that C2ORF40 mimic peptide fragment significantly suppressed cell proliferation of breast and lung cancer cells. Moreover, C2ORF40 mimic peptide fragment significantly inhibited the migration and invasion of breast cancer cells. Furthermore, we showed that this peptide suppressed tumorigenesis in breast tumor xenograft model. Cell cycle assay indicated that the C2ORF40 mimic peptide fragment suppressed the growth of tumor cells through inducing mitotic phase arrest. In conclusion, our results firstly suggested that this short synthetic peptide of human C2ORF40 may be a candidate tumor therapeutic agent.
Highlights
C2ORF40, named esophageal cancer related gene 4 (ECRG4) or proaugurin, is firstly found by Su et al in esophageal cancer [1]
Transcriptional analysis showed that the C2ORF40 mRNA level was significantly lower in 58 out of 70 breast cancer tissues (Figure 1A and 1B, Supplementary Figure 1A), which is consistent with our GEO data analysis [5]
We found a highly significant deficiency of C2ORF40 expression in all the breast cancer samples (P < 0.01) (Figure 1C and 1D), which was consistent with the quantitative real-time RT-PCR (qRT-PCR) results
Summary
C2ORF40 (chromosome 2 open reading frame 40), named esophageal cancer related gene 4 (ECRG4) or proaugurin, is firstly found by Su et al in esophageal cancer [1]. Our previous study indicated that DNA hypermethylation of the C2ORF40 promoter could downregulate its transcript level in human breast cancer cells [5]. Restoration of C2ORF40 expression could significantly suppress proliferation, migration and invasion of breast and other cancer cells [5, 12,13,14,15]. These data indicated that restoration of C2ORF40 could serve as therapeutic potential in human malignant tumors
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