Biological roles of filamin a in prostate cancer cells

• Autor(a) principal: Li,Xue-Chao
• Data de Publicação: 2019
• Outros Autores: Huang,Chuan-Xi, Wu,Shi-Kui, Yu,Lan, Zhou,Guang-Jian, Chen,Li-Jun
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: International Braz J Urol (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1677-55382019000500916
• topic: Prostatic Neoplasms; Filamins; RNAi Therapeutics

ABSTRACT Objective This study aims to investigate the association of filamin A with the function and morphology of prostate cancer (PCa) cells, and explore the role of filamin A in the development of PCa, in order to analyze its significance in the evolvement of PCa. Materials and Methods A stably transfected cell line, in which filamin A expression was suppressed by RNA interference, was first established. Then, the effects of the suppression of filamin A gene expression on the biological characteristics of human PCa LNCaP cells were observed through cell morphology, in vitro cell growth curve, soft agar cloning assay, and scratch test. Results A cell line model with a low expression of filamin A was successfully constructed on the basis of LNCaP cells. The morphology of cells transfected with plasmid pSilencer-filamin A was the following: Cells were loosely arranged, had less connection with each other, had fewer tentacles, and presented a fibrous look. The growth rate of LNCap cells was faster than cells transfected with plasmid pSilencer-filamin A (P <0.05). The clones of LNCap cells in the soft agar cloning assay was significantly fewer than that of cells stably transfected with plasmid pSilencer-filamin A (P <0.05). Cells stably transfected with plasmid pSilencer-filamin A presented with a stronger healing and migration ability compared to LNCap cells (healing rate was 32.2% and 12.1%, respectively; P <0.05). Conclusion The expression of the filamin A gene inhibited the malignant development of LNCap cells. Therefore, the filamin A gene may be a tumor suppressor gene.