Inhibition of focal adhesion kinase induces apoptosis in human osteosarcoma SAOS-2 cells

• DOI: 10.1007/s13277-013-1214-0
• Publication Date: 2013-10-03T01:27:01Z
• Authors: Jialiang Wang; Jianing Zu; Gongping Xu; Wei Zhao; Yan Jinglong
• Keywords: 0301 basic medicine; Osteosarcoma; Apoptosis; Bone Neoplasms; Flow Cytometry; 3. Good health; Gene Expression Regulation, Neoplastic; 03 medical and health sciences; Caspases; Cell Line, Tumor; Focal Adhesion Protein-Tyrosine Kinases; Humans; Cisplatin; RNA, Small Interfering; Cell Proliferation; Signal Transduction

Focal adhesion kinase (FAK), a non-receptor tyrosine protein, acts as an early modulator of integrin signaling cascade, regulating basic cellular functions. In transformed cells, unopposed FAK has been considered to promote tumor growth, progression, and metastasis. The aim this study was assess the role focal in human osteosarcoma SAOS-2 cells. cells were transfected with PGPU6/GFP/shNC, PGPU6/GFP/FAK-334 (shRNA-334), respectively. Expression detected by real-time PCR western blots. MTT assay used examine changes cell proliferation. Cell apoptosis analyzed flow cytometry. expression caspase-3,-7,-9 measured Western significantly decreased shRNA-334 group contrast control (P < 0.01). Cells proliferation inhibited + cisplatin, effects clearly enhanced when treated anticancer agents. level cisplatin higher than current data support evidence that down-regulation could induce through caspase-dependent death pathway. Inhibition kinases may be important for therapies designed enhance osteosarcoma.