Inhibition of CDC42 reduces macrophage recruitment and suppresses lung tumorigenesis in vivo
| Autor: | Yanhui Xu, Lei Zhang, Bo Zhang, Guoping Chen, Lilong Xia, Xinhai Zhu, Jing Luo, Jian Zhang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Cell division Carcinogenesis Macrophage invasion Apoptosis CDC42 Biology medicine.disease_cause Biochemistry Pathogenesis Carcinoma Lewis Lung Mice 03 medical and health sciences 0302 clinical medicine Cell Movement In vivo medicine Animals RNA Small Interfering cdc42 GTP-Binding Protein Molecular Biology Cells Cultured Cell Proliferation Lung Macrophages Cell Biology Mice Inbred C57BL Disease Models Animal 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Cancer research human activities Macrophage recruitment |
| Zdroj: | Journal of Receptors and Signal Transduction. 41:504-510 |
| ISSN: | 1532-4281 1079-9893 |
| DOI: | 10.1080/10799893.2020.1828916 |
| Popis: | Cell division control (CDC) 42 has been involved in the regulation of diverse cancers. Macrophage recruitment plays an important role in the pathogenesis and development of tumor. However, it remains unclear whether CDC42 contributes to macrophage recruitment and lung tumorigenesisSmall interference RNA (siRNA) was used to knock down CDC42 in the Lewis lung carcinoma (LLC)1. The invasion capability of CDC42 knockdown LLC1 cells was evaluated. LLC1 cells with CDC42 targeted small hairpin RNA (shRNA) were inoculated into C57BL/6 mice to establish the tumor-bearing animal model Tumor size and metastasis related proteins were measured. In addition, the invasion of macrophages in the tumor site as well as macrophage chemokine were also determined in the model.The capacity of invasion and metastasis of LLC1 cells significantly decreased when CDC42 was knocked down. When inoculated with CDC42 knockdown LLC1 cellsOur data suggest that the inhibition of CDC42 expression in lung cancer cells can significantly prevent the pathogenesis and development of tumor in an allograft tumor model |
| Databáze: | OpenAIRE |
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