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Therapeutic Peptide RF16 Derived from CXCL8 Inhibits MDA-MB-231 Cell Invasion and Metastasis
Chun-Ming Chang1,2, Chun-Chun Chang3,4, Ho Yin Pekkle Lam5,6
1Department of General Surgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 97004, Taiwan.
Abstract:
Interleukin (IL)-8 plays a vital role in regulating inflammation and breast cancer formation by activating CXCR1/2. We previously designed an antagonist peptide, (RF16), to inhibits the activation of downstream signaling pathways by competing with IL-8 in binding to CXCR1/2, thereby inhibiting IL-8-induced chemoattractant monocyte binding. To evaluate the effect of the RF16 peptide on breast cancer progression, triple-negative MDA-MB-231 and ER-positive MCF-7 breast cancer cells were used to investigate whether RF16 can inhibit the IL-8-induced breast cancer metastasis. Using growth, proliferation, and invasiveness assays, the results revealed that RF16 reduced cell proliferation, migration, and invasiveness in MDA-MB-231 cells. The RF16 peptide also regulated the protein and mRNA expressions of epithelial-mesenchymal transition (EMT) markers in IL-8-stimulated MDA-MB-231 cells. It also inhibited downstream IL-8 signaling and the IL-8-induced inflammatory response via the mitogen-activated protein kinase (MAPK) and Phosphoinositide 3-kinase (PI3K) pathways. In the xenograft tumor mouse model, RF16 synergistically reinforces the antitumor efficacy of docetaxel by improving mouse survival and retarding tumor growth. Our results indicate that RF16 significantly inhibited IL-8-stimulated cell growth, migration, and invasion in MDA-MB-231 breast cancer cells by blocking the activation of p38 and AKT cascades. It indicated that the RF16 peptide may serve as a new supplementary drug for breast cancer.
Insights
The RF16 peptide inhibits breast cancer progression by blocking Interleukin-8 (IL-8) signaling. This novel peptide reduces cancer cell growth, migration, and invasion, offering potential as a supplementary breast cancer treatment.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Interleukin-8 (IL-8) is a key regulator of inflammation and breast cancer progression.
- IL-8 activates CXCR1/2, promoting cancer cell proliferation, migration, and invasion.
- Targeting the IL-8 pathway presents a therapeutic strategy for breast cancer.
Purpose of the Study:
- To evaluate the efficacy of the antagonist peptide RF16 in inhibiting IL-8-induced breast cancer metastasis.
- To investigate RF16's effects on breast cancer cell lines MDA-MB-231 and MCF-7.
- To explore RF16's impact on IL-8 signaling pathways and epithelial-mesenchymal transition (EMT).
Main Methods:
- Cell proliferation, migration, and invasion assays were performed on MDA-MB-231 and MCF-7 cells.
- Analysis of epithelial-mesenchymal transition (EMT) marker expression at protein and mRNA levels.
- Inhibition of downstream IL-8 signaling pathways, including MAPK and PI3K.
- Evaluation of RF16's synergistic effect with docetaxel in a xenograft tumor mouse model.
Main Results:
- RF16 significantly reduced cell proliferation, migration, and invasiveness in MDA-MB-231 cells.
- RF16 modulated EMT markers and inhibited IL-8-induced inflammatory responses.
- RF16 blocked p38 and AKT pathway activation, inhibiting IL-8 signaling.
- In vivo, RF16 enhanced docetaxel's antitumor efficacy, improving survival and reducing tumor growth.
Conclusions:
- The RF16 peptide effectively inhibits IL-8-stimulated breast cancer cell growth, migration, and invasion.
- RF16 acts by blocking the IL-8/CXCR1/2 axis and downstream signaling pathways.
- RF16 demonstrates potential as a novel supplementary therapeutic agent for breast cancer treatment.
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