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An antitumor peptide RS17-targeted CD47, design, synthesis, and antitumor activity
Xinmin Wang1,2, Ying Wang1,2, Jialiang Hu1,2
1The Engineering Research Centre of Peptide Drug Discovery and Development, China Pharmaceutical University, Nanjing, Jiangsu, China.
Background:
CD47 is a widely expressed transmembrane protein located on the surface of somatic cells. It mediates a variety of cellular processes including apoptosis, proliferation, adhesion, and migration. An important role for CD47 is the transmission of a "Don't eat me" signal by interacting with SIRPα on the macrophage surface membrane, thereby preventing the phagocytosis of normal cells. However, cancer cells can take advantage of this autogenous signal to protect themselves from phagocytosis, thus enabling immune escape. Blocking the interaction between CD47 and SIRPα has proven to be effective in removing cancer cells. The treatment of various cancers with CD47 monoclonal antibodies has also been validated.
Methods:
We designed and synthesized a peptide (RS17), which can specifically bind to CD47 and block CD47-SIRPα signaling. The affinity of RS17 for CD47-expressing tumor cells was determined, while the inhibition of CD47-SIRPα signaling was evaluated in vitro and in vivo.
Results:
The results indicated that RS17 significantly promotes the phagocytosis of tumor cells by macrophages and had a similar therapeutic effect compared with a positive control (CD47 monoclonal antibodies). In addition, a cancer xenograft mouse model was established using CD47-expressing HepG2 cells to evaluate the effect of RS17 on tumor growth in vivo. Using ex vivo and in vivo mouse models, RS17 demonstrated a high inhibitory effect on tumor growth.
Conclusions:
Based on our results, RS17 may represent a novel therapeutic peptide for cancer therapy.
Insights
A new peptide, RS17, blocks the CD47-SIRPα "Don't eat me" signal, enhancing macrophage cancer cell engulfment. This peptide shows significant tumor growth inhibition in preclinical models, offering a potential new cancer therapy.
Area of Science:
- Immunology
- Oncology
- Biochemistry
Background:
- CD47 is a transmembrane protein mediating cellular processes and immune evasion by sending a "Don't eat me" signal via SIRPα interaction.
- Cancer cells exploit the CD47-SIRPα pathway to evade phagocytosis, contributing to immune escape.
- Blocking CD47-SIRPα interaction is a validated strategy for cancer cell removal.
Purpose of the Study:
- To design and synthesize a novel peptide, RS17, that specifically binds to CD47 and inhibits CD47-SIRPα signaling.
- To evaluate the in vitro and in vivo efficacy of RS17 in blocking CD47-SIRPα signaling and promoting tumor cell phagocytosis.
Main Methods:
- Synthesis of RS17 peptide designed to block CD47-SIRPα interaction.
- Determination of RS17 affinity for CD47-expressing tumor cells.
- In vitro and in vivo evaluation of CD47-SIRPα signaling inhibition.
- Assessment of RS17's effect on tumor cell phagocytosis by macrophages.
- Establishment of a cancer xenograft mouse model (HepG2 cells) to evaluate in vivo tumor growth inhibition.
Main Results:
- RS17 significantly enhances macrophage-mediated phagocytosis of tumor cells.
- RS17 demonstrated comparable therapeutic effects to CD47 monoclonal antibodies in preclinical settings.
- In vivo studies using a cancer xenograft mouse model showed that RS17 effectively inhibits tumor growth.
Conclusions:
- RS17 peptide successfully blocks CD47-SIRPα signaling, promoting anti-tumor immunity.
- RS17 exhibits significant therapeutic potential for cancer treatment, comparable to existing antibody therapies.
- RS17 represents a promising novel peptide-based therapeutic candidate for various cancers.
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