1. Stable knockdown of TPPP3 by RNA interference in Lewis lung carcinoma cell inhibits tumor growth and metastasis
- Author
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Renming Hu, Jiada Li, Xuanchun Wang, and Wenbai Zhou
- Subjects
Male ,Clinical Biochemistry ,Cell ,Biology ,medicine.disease_cause ,Carcinoma, Lewis Lung ,Mice ,RNA interference ,Cell Line, Tumor ,medicine ,Animals ,Neoplasm Metastasis ,Molecular Biology ,Mitosis ,DNA Primers ,Base Sequence ,Cell growth ,Lewis lung carcinoma ,Cell Biology ,General Medicine ,Cell cycle ,Cell biology ,Mice, Inbred C57BL ,medicine.anatomical_structure ,Tumor progression ,Gene Knockdown Techniques ,Cancer research ,RNA Interference ,Carcinogenesis ,Cell Adhesion Molecules ,Cell Division - Abstract
Tubulin polymerization promoting protein 3 (TPPP3), a member of the TPPP family, can induce tubulin polymerization and microtubule bundling. Previously, it has been shown that TPPP3 plays an important role in cell proliferation. Depletion of TPPP3 by microRNA-based RNA interference (RNAi) inhibits cell growth, arrests cell cycles, and causes mitotic abnormalities in HeLa cells. In the present study, we knocked down TPPP3 in Lewis lung carcinoma (LLC) cells with the same RNAi construct, and observed a retarded tumor cell growth in vitro. Furthermore, C57BL/6 mice that received subcutaneously injected LLC cells in which TPPP3 was knocked down showed a pronounced reduction in tumor progression. The migration/invasion activity of TPPP3-knockdown LLC cells was significantly suppressed in a transwell chamber migration assay. When these cells were injected into the tail veins of C57BL/6 mice, they exhibited milder lung metastasis compared with control tumor cells. Taken together, these findings suggested that the TPPP3 gene played an important role in tumorigenesis and metastasis, and it could potentially become a novel target for cancer therapy.
- Published
- 2010