Upregulation of Id3 inhibits cell proliferation and induces apoptosis in A549/DDP human lung cancer cells in vitro

摘要

Inhibitor of DNA binding (Id) 3 is a member of the Id multigene family of dominant-negative helix-loop-helix transcription factors, which function as oncogenes or tumor suppressors in human cancers. Its upregulation was recently shown to have inhibitory effects on lung cancer, which is the leading cause of cancer-associated mortality worldwide. As drug resistance represents a major bottleneck of cancer therapy, the present study assessed the ability of Id3 to inhibit cisplatin-resistant A549 lung adenocarcinoma cells (A549/DDP). A549/DPP cells were transiently transfected with enhanced green fluorescence protein overexpression plasmid (pEGFP) or Id3 overexpression plasmid (Id3/pEGFP), which was confirmed by confocal fluorescence microscopy, PCR and western blot analysis. The effects of Id3 on the viability and apoptosis of A549/DDP were determined using an MTT assay, fluorescence microscopy with Hoechst 33258 staining and flow cytometry following Annexin V/propidium iodide double staining. The results revealed that overexpression of Id3 significantly inhibited the proliferation and viability of A549/DDP cells in a time-dependent manner. Furthermore, overexpression of Id3 significantly increased the apoptotic rate of A549/DDP cells from 2.73 to 16.92%, confirming the implication of Id3 in the negative control of tumour growth. The results of the present study revealed that overexpression of Id3 may serve as a novel strategy for inhibiting cisplatin-sensitive lung cancer. Further experiments will be performed to determine whether Id3 overexpression could enhance the sensitivity of lung cancer cells to DDP.