Original Article

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

Shuang-shuang Wu, Wei Xu, Shan Liu, Bo Chen, Xue-li Wang, Yan Wang, Shi-feng Liu, Jian-qing Wu
DOI: 10.1038/aps.2010.216

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.
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