Knocking down Dp71 expression in A549 cells reduces its malignancy in vivo and in vitro. (2nd January 2016)

• Record Type: Journal Article
• Authors: Tan, Sichuang; Tan, Sipin; Chen, Zhikang; Cheng, Ke; Chen, Zhicao; Wang, Wenmei; Wen, Qiaocheng; Zhang, Weilin
• Is Part Of: Cancer investigation. Volume 34:Number 1(2016)
• Page Start: 16
• Page End: 25
• Publication Date: 2016-01-02
• Subjects: Dp71 -- Knockdown -- A549 -- Malignancy; Cancer -- Periodicals; Oncology -- Periodicals; Medical Oncology -- Periodicals; Neoplasms -- Periodicals; 616.994
• DOI: 10.3109/07357907.2015.1084002
• Languages: English
• ISSNs: 0735-7907

Abstract

ABSTRACT: Dp71 is one of the most ubiquitously expressed isoforms of dystrophin, the pathological genes of DMD. In order to find whether the alteration of Dp71 can affect the phenotypes of cell other than PC12, an A549 cell line with stably transfected Dp71 siRNA plasmids was set up and named A549-Dp71AS cell. It is demonstrated for the first time that the A549-Dp71AS cell line displayed decreased invasion capabilities, reduced migration ability, decreased proliferation rate, and lessened clonogenic formation. Cisplatin-induced apoptosis was also increased in A549-Dp71AS cell line via enhancing the Caspase 3, Caspase 8, and Caspase 9 activities. Knocking down Dp71 expression can significantly inhibit the A549 xenograft tumor growth in nude mice. The A549-Dp71AS cells and xenograft tumor tissues displayed reduced lamin B1, Bcl-2, and MMP2 protein expression, which accounts for the reduced malignancy of A549-Dp71AS cells in vivo and in vitro .