Vol. 45 (5): 916-924, September – October, 2019
doi: 10.1590/S1677-5538.IBJU.2018.0535
ORIGINAL ARTICLE
Xue-Chao Li 1, Chuan-Xi Huang 2, Shi-Kui Wu 1, Lan Yu 3, Guang-Jian Zhou 3, Li-Jun Chen 1
1 Department of Urology, the Fifth Medical Center, Chinese PLA General Hospital, Beijing, China; 2 College of Life Science, Hebei University, Hebei, China; 3 Laboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China
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.
Keywords: Prostatic Neoplasms; Filamins; RNAi Therapeutics
