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Down-regulation of ALKBH2 increases cisplatin sensitivity in H1299 lung cancer cells

  
@article{APS6717,
	author = {Shuang-shuang Wu and Wei Xu and Shan Liu and Bo Chen and Xue-li Wang and Yan Wang and Shi-feng Liu and Jian-qing Wu},
	title = {Down-regulation of ALKBH2 increases cisplatin sensitivity in H1299 lung cancer cells},
	journal = {Acta Pharmacologica Sinica},
	volume = {32},
	number = {3},
	year = {2016},
	keywords = {},
	abstract = {Aim: To elucidate the combined effect of alkylated DNA repair protein alkB homolog 2 (ALKBH2)-targeting gene therapy and cisplatin (cDDP) chemotherapy on the non-small cell lung cancer (NSCLC) H1299 cell line.
Methods: ALKBH2 was down-regulated in H1299 cells by lentivirus-mediated RNA interference (RNAi). Changes in ALKBH2 expression were determined using real-time RT-PCR and Western blotting. Cell viability was evaluated using MTT assay. DNA synthesis in proliferating cells was determined using BrdU incorporation assay. Cell apoptosis was determined using flow cytometry.
Results: Lentivirus-mediated ALKBH2 silencing alone did not induce apoptosis or attenuate the growth potential of H1299 cells within five days post-infection. Combined treatment modalities with lentivirus-mediated ALKBH2 down-regulation and cDDP (333 μmol/L) were significantly more potent in inhibiting cell growth and inducing apoptosis than mono-chemotherapy.
Conclusion: Combined treatment modalities of ALKBH2 knockdown and cDDP chemotherapy have the potential to improve the efficacy in the treatment of NSCLC.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/6717}
}