| Literature DB >> 26691328 |
Sichuang Tan1, Sipin Tan2,3, Zhikang Chen4, Ke Cheng5, Zhicao Chen5, Wenmei Wang2, Qiaocheng Wen4, Weilin Zhang4.
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.Entities:
Keywords: A549; Dp71; Knockdown; Malignancy
Mesh:
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Year: 2015 PMID: 26691328 DOI: 10.3109/07357907.2015.1084002
Source DB: PubMed Journal: Cancer Invest ISSN: 0735-7907 Impact factor: 2.176