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Procedures: Procedures: Pleura |

Experimental Study of Focal Adhesion Kinase (FAK) and Insulin-Like Growth Factor-I Receptor (IGF-1R) in Malignant Pleural Effusions FREE TO VIEW

Shun Liu; Wei Zhang; Yi Huang; Feng Wu; Lan Zhu; Ling Gong; Chuan Huang
Author and Funding Information

The Institute of Respiratory Diseases in Zunyi City, The First People's Hospital of Zunyi City, Zunyi, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A444. doi:10.1016/j.chest.2016.02.462
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SESSION TITLE: Procedures: Pleura

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: This study is aimed to explore the role of focal adhesion kinase (FAK) and the insulin- like growth factor-I receptor (IGF-1R) in malignant pleural effusion (MPE).

METHODS: FAK and IGF-1R in pleural effusion (BPE) and malignant pleural effusion (MPE) were detected by ELISA. The FAK and IGF-1R mRNA were measured by RT-PCR;The expression of IGF-1R, FAK, pIGF-1R, pFAK were detected through Western-blot. The effection of TAE226 on cell migration, invasion, apoptosis were tested by Matrigel Invasion Assay, Wound healing and TUNEL. We established an orthotopic transplantation model of MPE in SCID mice by injecting A549 cells thoracically. We watched gross morphology of tumor tissue in HE staining, assayed CD31 and ki67 expression in tumors tissue in Immunohistochemical staining.

RESULTS: FAK and IGF-1R protein were much more highly expressed in MPE than in BPE in the ELISA detection. The RT-PCR indicated that FAK mRNA expression in A549 cells and NCI-H1650 cells was higher than in C57/BL6 cells and L929 cells. Meanwhile we also explored that IGF-1R mRNA was more highly expressed in A549 cells than in NCI-H1650 cells, C57 BL/c cells, L929 cells. In RT-PCR experiments, we found that the expression of FAK mRNA and IGF-1R mRNA were depressed after treated with TAE 226. We also got that the expression of pFAK and pIGF-1R protein were significantly suppressed after A549 cells exposed to TAE 226. The cell proliferation was inhibited with concentration dependent. Then A549 cells were treated with TAE 226 for 24hr, cell Proliferation was dramatically depressed. When A549 cells were given with TAE226, we found that the cell migration and invasion were significantly inhibited and its apoptosis was increased. Treatment with TAE226 significant inhibited tumor growth and MPE production.

CONCLUSIONS: Our work demonstrated that FAK and IGF-1R played an efficient role in MPE produced; TAE226 through suppressive FAK and IGF-1R which can suppressive effect on angiogenesis and tumor growth, so can inhibitied MPE produce, which provided a certain theoretical basis for the effectiveness of TAE226 on the MPE treatment. By in vivo, in vitro experiments, it is clarified that FAK and IGF-1R not merely is a critical factor of angiogenesis in chest malignant tumor, but also involves in the development and progression of MPE. And it would provide a extremely novel potential targets for pulmonary MPE.

CLINICAL IMPLICATIONS: This study would provide a extremely novel potential targets for pulmonary MPE.

DISCLOSURE: The following authors have nothing to disclose: Shun Liu, Wei Zhang, Yi Huang, Feng Wu, Lan Zhu, Ling Gong, Chuan Huang

No Product/Research Disclosure Information


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