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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
N-terminal polypeptide derived from vMIP-II exerts its antitumor activity by inhibiting the CXCR4 pathway in human
Qingling Yang1, Haihua Wu2, Haifeng Wang2
1Hefei National Laboratory for Physical Sciences at Microscale and the Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230026, P.R. China.
Abstract:
Emerging evidence demonstrates that the stromal derived factor-1 (SDF-1α)/CXCR4 axis is associated with tumor aggressiveness and metastasis, including glioma, the most common brain cancer. In the present study, we demonstrated that a novel designed peptide NT21MP of viral macrophage inflammatory protein II, targeting CXCR4 inhibits SDF-1α-induced activation in glioma. The effects of NT21MP on CXCR4 expression, cell survival and migration were assessed on the human glioma cell line U251 and SHG-44 exposed to SDF-1α, by western blotting, MTT assay, flow cytometry and transwell migration assay. Our results illustrated that NT21MP inhibited SDF-1α induced proliferation, migration and invasion by upregulated pro-apoptotic genes (Bak1 and caspase-3) and downregulated Bcl-2/Bax as well as cell cycle regulators (cyclin D1 and CDK4) to arrest cell cycle in G0/G1 phase and promote apoptosis. By RT-qPCR and immunofluorescence we found that CXCR4 was highly expressed in SHG-44 cells. Our results from wound healing and transwell invasion assays indicated silencing of CXCR4 significantly inhibited the SDF-1α‑induced migration and invasion; similarly, flow cytometry showed that treatment with si-CXCR4 affected cell cycle and induced cell apoptosis in SHG-44. However, these effects were significantly weakened by NT21MP. In conclusion, the present study indicates that NT21MP plays a regulatory role in the SDF-1α/CXCR4 axis and further manages the invasion, migration, apoptosis and cell cycle of glioma cells. Thus, NT21MP might represent a novel therapeutic approach against glioma.
Insights
A novel peptide, NT21MP, targets the stromal derived factor-1 (SDF-1α)/CXCR4 pathway to inhibit glioma cell invasion and migration. This peptide promotes apoptosis and arrests the cell cycle, offering a potential new therapy for brain cancer.
Area of Science:
- Oncology
- Molecular Biology
- Neuroscience
Background:
- The stromal derived factor-1 (SDF-1α)/CXCR4 signaling pathway is implicated in the aggressiveness and metastasis of various cancers, including glioma.
- Glioma, the most common primary brain cancer, exhibits high levels of CXCR4 expression, suggesting its potential role in tumor progression.
Purpose of the Study:
- To investigate the inhibitory effects of a novel peptide, NT21MP, on the SDF-1α/CXCR4 axis in human glioma cells.
- To evaluate NT21MP's impact on glioma cell survival, migration, invasion, cell cycle progression, and apoptosis.
Main Methods:
- Human glioma cell lines (U251 and SHG-44) were treated with SDF-1α and/or NT21MP.
- Techniques included western blotting, MTT assay, flow cytometry, RT-qPCR, immunofluorescence, wound healing, and transwell migration/invasion assays.
- CXCR4 expression was assessed, and its silencing was performed using si-CXCR4.
Main Results:
- NT21MP effectively inhibited SDF-1α-induced proliferation and migration in glioma cells.
- The peptide upregulated pro-apoptotic genes (Bak1, caspase-3), downregulated Bcl-2/Bax, and arrested the cell cycle in the G0/G1 phase.
- Silencing CXCR4 inhibited migration and invasion, but these effects were attenuated by NT21MP, indicating its regulatory role.
Conclusions:
- NT21MP demonstrates a significant regulatory role in the SDF-1α/CXCR4 axis, impacting glioma cell invasion, migration, apoptosis, and cell cycle.
- The findings suggest NT21MP holds promise as a novel therapeutic strategy for treating glioma.
