GLIPR1 modulates the response of cisplatin-resistant human lung cancer cells to cisplatin
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Xin Gong1, Jing Liu2, Dan Zhang1
1Department of Pulmonary Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Background And Objective:
Chemotherapy drugs, such as cisplatin (DDP), improve the survival of patients with lung cancer by inducing apoptosis in cancer cells, which quickly develop resistance to DDP through uncharacterized mechanisms. Glioma Pathogenesis-Related Protein 1 (GLIPR1) plays an important role in cell proliferation, migration and apoptosis. However, the expression and function of GLIPR1 in mediating DDP resistance in human lung adenocarcinoma A549/DDP and human large cell lung cancer H460/DDP cells has not yet been reported.
Methods:
In this study, real-time PCR (RT-PCR) and western blot were used to examine the mRNA and protein expression of GLIPR1, respectively. Bright-field microscopy, the cell counting kit-8 (CCK-8) assay, flow cytometry analysis and JC-1 dye were used to measure the cellular morphology, proliferation, apoptosis and mitochondrial membrane potential, respectively.
Results:
Compared to human lung adenocarcinoma A549 cells, the mRNA and protein expression of GLIPR1 were significantly increased in DDP-resistant A549/DDP cells (p < 0.05). Similarly, the mRNA level of GLIPR1 in DDP-resistant H460/DDP cells was also significantly higher than that in DDP-sensitive H460 cells (p < 0.05). Silencing of GLIPR1 in A549/DDP and H460/DDP cells led to increased apoptosis via a mitochondrial signaling pathway following incubation with various concentrations of DDP. Furthermore, GLIPR1 downregulation markedly reduced the protein expression of Bcl-2, and increased the cleaved Poly (ADP-Ribose) Polymerase (PARP) and cleaved caspase-3 in DDP-resistant A549/DDP cells.
Conclusion:
In this study, we demonstrated for the first time that GLIPR1 could modulate the response of DDP-resistant A549/DDP and H460/DDP cells to cisplatin. Therefore, GLIPR1 deserves further investigation in the context of none-small lung cancer (NSCLC).
Insights
Glioma Pathogenesis-Related Protein 1 (GLIPR1) is upregulated in cisplatin-resistant lung cancer cells. Silencing GLIPR1 enhances apoptosis and overcomes cisplatin resistance, suggesting GLIPR1 as a therapeutic target for non-small cell lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Cisplatin (DDP) is a chemotherapy drug used for lung cancer.
- Lung cancer cells develop resistance to DDP through unknown mechanisms.
- Glioma Pathogenesis-Related Protein 1 (GLIPR1) influences cell proliferation, migration, and apoptosis.
Purpose of the Study:
- To investigate the role of GLIPR1 in DDP resistance in human lung adenocarcinoma (A549/DDP) and large cell lung cancer (H460/DDP) cells.
- To determine if GLIPR1 expression is altered in DDP-resistant lung cancer cells.
- To elucidate the functional impact of GLIPR1 on DDP sensitivity and apoptosis.
Main Methods:
- Real-time PCR (RT-PCR) and Western blot to assess GLIPR1 mRNA and protein expression.
- Cell Counting Kit-8 (CCK-8) assay for cell proliferation.
- Flow cytometry and JC-1 dye to analyze apoptosis and mitochondrial membrane potential.
Main Results:
- GLIPR1 mRNA and protein expression were significantly higher in DDP-resistant A549/DDP and H460/DDP cells compared to their sensitive counterparts.
- Silencing GLIPR1 in resistant cells increased DDP-induced apoptosis via the mitochondrial pathway.
- GLIPR1 downregulation reduced Bcl-2 expression and increased cleaved PARP and cleaved caspase-3.
Conclusions:
- GLIPR1 plays a role in mediating DDP resistance in lung cancer cells.
- GLIPR1 modulates the apoptotic response to cisplatin in resistant lung cancer cells.
- GLIPR1 is a potential therapeutic target for overcoming DDP resistance in non-small cell lung cancer (NSCLC).
