Knockdown of integrin α3β1 expression induces proliferation and migration of non-small cell lung cancer cells
| Autor: | Dong-Wan Seo, Young-Rak Cho, Hyun Jae Yoon, Ji-Hye Joo |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
MAPK/ERK pathway
Cancer Research Lung Neoplasms MAP Kinase Signaling System Cell Integrin Biology Transfection Cell Movement Carcinoma Non-Small-Cell Lung medicine Humans RNA Small Interfering Protein kinase B Cell Proliferation Cell growth Integrin alpha3beta1 NF-kappa B General Medicine Cell cycle Cyclin-Dependent Kinases Cell biology Up-Regulation ErbB Receptors medicine.anatomical_structure Oncology Matrix Metalloproteinase 9 Proto-Oncogene Proteins c-bcl-2 Cancer cell Cancer research biology.protein Matrix Metalloproteinase 2 RNA Interference Tumor Suppressor Protein p53 A431 cells Proto-Oncogene Proteins c-akt |
| Zdroj: | Oncology reports. 29(2) |
| ISSN: | 1791-2431 |
| Popis: | Integrin α3β1 is expressed on many types of cancer cells and can regulate tumor growth and progression. In the present study, we examined the roles and molecular mechanism of integrin α3β1 in modulating cell proliferation and migration of p53-deficient non-small cell lung cancer (NSCLC) cells. Reduced expression of integrin α3 by RNA silencing clearly induces cell proliferation and migration in H1299 cells, compared with those in control cells. Enhanced proliferation in integrin α3-silenced cells is mediated by upregulation and nuclear localization of cyclin-dependent kinases, and these effects require the activation of Akt and ERK as evidenced by treatment with LY294002 and PD98059, respectively. Furthermore, suppression of integrin α3 expression induces the expression of nuclear factor-κB and Bcl-2 as well as epidermal growth factor receptor, which are positively correlated with cell proliferation and survival. In contrast, increase in cell migration of integrin α3-silenced cells is found to be independent of Akt or ERK signaling pathways. Collectively, these findings suggest that integrin α3β1 plays pivotal roles in regulating cell proliferation and migration that enhance the invasive type of p53-deficient NSCLC cells. |
| Databáze: | OpenAIRE |
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