Autophagic inhibitor attenuates rapamycin-induced inhibition of proliferation in cultured A549 lung cancer cells

R.-y. Jiang, H.-l. Pei, W.-d. Gu, J. Huang, Z.-g. Wang

Department of Radiation Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China. wangzhigang2012@126.com

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• Oncology

BACKGROUND: Increasing studies have suggested that rapamycin has inhibitory effect for cancer cell proliferation.

AIM: The present study aimed to investigate the effect of rapamycin on the proliferation of A549 lung cancer cells and try to elucidate its probable mechanism.

MATERIALS AND METHODS: A549 cells were randomly divided into the following 3 groups (n=6): the Dulbecco’s modified Eagle’s medium (DMEM) culture solution administered alone group (C group), the 10 nmol/l rapamycin administered alone group (R group) and the 5 mmol/l 3-methyladenine (3-MA) plus 10 nmol/l rapamycin administered group (MR group). Death percentage of A549 cells was observed and the levels of caspase-3, Beclin-1, and microtubule-associated protein 1 light chain 3-II (LC3-II) were determined.

RESULTS: Compared with C group, percentage of cell death, caspase-3, Beclin-1 and LC3-II both showed a significant increase in R group (p < 0.05). On the contrary, as compared with R group, percentage of cell death, caspase-3, Beclin-1 and LC3-II both showed a significant decrease in MR group (p < 0.05).

CONCLUSIONS: Rapamycin has an inhibitory effect for the proliferation of A549 cells, and its mechanism is likely related to the activation of autophagic pathway.

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