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Antisense oligonucleotides targeting midkine inhibit tumor growth in an in situ human hepatocellular carcinoma model

  
@article{APS4378,
	author = {Li-cheng Dai and Xiang Wang and Xing Yao and Li-shan Min and Jin-liang Ping and Jian-fang He},
	title = {Antisense oligonucleotides targeting midkine inhibit tumor growth in an in situ human hepatocellular carcinoma model},
	journal = {Acta Pharmacologica Sinica},
	volume = {28},
	number = {3},
	year = {2016},
	keywords = {},
	abstract = {Aim:  To evaluate the in vivo antitumor effects of antisense oligonucleotides targeting midkine (MK-AS). Methods:  An in situ human hepatocellular carcinoma (HCC) model was established in mice livers orthotopically. The MK-AS and 5-fluorouracil (5-Fu) were administered intravenously. The tumor sizes and plasma alpha-fetoprotein (AFP) were measured by calipers and radiation immunoassay respectively. The morphology of tumors was evaluated by hematoxylin-eosin staining of histological sections. Human MK, p53, Bax, Bcl-2, and caspase-3 protein content were detected by Western blotting. Results:  MK-AS significantly inhibited in situ  human HCC growth in mice compared with the saline group in a dose-dependent manner. After the treatment with MK-AS or with 5-Fu, the plasma AFP concentration decreased in a dose-dependent manner. Interestingly, MK-AS also clearly downregulated the protein level of Bcl-2, and upregulated p53, Bax, and caspase-3 in the hepatocellular carcinoma tissue. Conclusion:  These results demonstrated that MK-AS was an effective antitumor antisense oligonucleotide  in vivo in mice; its antitumor effect is associated with the increase of pro-apoptotic proteins, such as p53, Bax, and caspase-3, and the decrease of the anti-apoptotic protein, Bcl-2.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/4378}
}