Overexpression of CAP1 and its significance in tumor cell proliferation, migration and invasion in glioma

• Published in: Oncology reports Vol. 36; no. 3; pp. 1619 - 1625
• Main Authors: Fan, Yue-Chao, Cui, Chen-Chen, Zhu, Yi-Shuo, Zhang, Lei, Shi, Meng, Yu, Jin-Song, Bai, Jin, Zheng, Jun-Nian
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.09.2016; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Adult; Biomarkers, Tumor - analysis; Brain cancer; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Brain research; CAP1; Care and treatment; Cell adhesion & migration; Cell Cycle Proteins - metabolism; Cell growth; Cell Movement - physiology; Cell Proliferation - physiology; Cellular proteins; Cytoskeletal Proteins - metabolism; Development and progression; Female; Gene expression; Gene Knockdown Techniques; Genetic aspects; Glioma; Glioma - metabolism; Glioma - pathology; Gliomas; Health aspects; Humans; Immunohistochemistry; invasion; Male; Medical prognosis; Metastasis; Middle Aged; migration; Morphology; Neoplasm Invasiveness - pathology; proliferation; Properties; Proteins; Studies; Tissue Array Analysis; Tumors; Up-Regulation; China
• ISSN: 1021-335X; 1791-2431
• DOI: 10.3892/or.2016.4936

Adenylate cyclase-associated protein 1 (CAP1), a protein related to the regulation of actin filaments and the Ras/cAMP pathway, is associated with tumor progression. Nevertheless, the expression level and effects of CAP1 in regards to glioma have not been reported. In the present study, we examined the expression of CAP1 in glioma and tumor adjacent normal brain tissues by tissue microarray and immunohistochemistry. Our results showed that CAP1 was overexpressed in glioma tissues in comparison with that noted in the tumor adjacent normal brain tissues and increased staining of CAP1 was found to be correlated with WHO stage. In addition, we discovered that knockdown of CAP1 by specific RNA interference markedly inhibited cell growth and caused downregulation of the proliferation markers, PCNA and cyclin A. We further demonstrated that knockdown of CAP1 inhibited cell metastatic abilities by downregulating N-cadherin and vimentin and upregulating E-cadherin. These findings revealed that CAP1 expression is markedly increased in human glioma and that downregulation of CAP1 in tumors may serve as a treatment for glioma patients.