2014Oncology ReportsOpen access

Interferon-λ1 induces G1 phase cell cycle arrest and apoptosis in gastric carcinoma cells in vitro

Zhitao Gao, Mo‐Li Zhu, Yaping Wu, Pan Gao, Zhihai Qin, Hui Wang

Open full text 13 citations

Abstract

The aim of the present study was to examine the potential antitumor action of IFN-λ1 in human gastric carcinoma cell lines and the possible interaction between IFN-λ1 and human gastric carcinoma cells. Gastric carcinoma HGC-27 and SGC-7901 cells were treated with IFN-λ1 (0, 10, 100, 1000 ng/ml) for 48 h. Cytotoxicity was examined using an MTT method. Cell cycle distribution was examined using propidium iodide staining. Apoptosis was examined using the Annexin V-FITC/PI apoptosis kit. By using flow cytometry and JC-1 probe, the mitochondrial membrane potential of cells following treatment with IFN-λ1 was also examined. Expression levels of representative apoptosis‑related proteins were evaluated by western blot analysis. IFN-λ1 inhibited the proliferation of gastric carcinoma cells in a concentration‑dependent manner. IFN-λ1 increased the accumulation of cells in the sub-G0 phase and arrested the cells in the G1 phase. Exposure to IFN‑λ1 decreased the mitochondrial membrane potential and increased apoptosis. Moreover, IFN‑λ1 exposure upregulated the expression of p21, p27 and Bax, downregulated the expression of Bcl‑2, increased the release of cytochrome c and apoptosis-inducing factor (AIF) and activated caspase-3 and caspase-9. In conclusion, IFN-λ1 inhibits the proliferation of gastric carcinoma cells by arresting the cells in the G1 phase and by inducing mitochondrial‑mediated apoptosis.

Open-access reader

About this research paper

What this paper is about

The aim of the present study was to examine the potential antitumor action of IFN-λ1 in human gastric carcinoma cell lines and the possible interaction between IFN-λ1 and human gastric carcinoma cells. Gastric carcinoma HGC-27 and SGC-7901 cells were treated with IFN-λ1 (0, 10, 100, 1000 ng/ml) for 48 h. Cytotoxicity was examined using an MTT method. Cell cycle distribution was examined using propidium iodide staining. Apoptosis was examined using the Annexin V-FITC/PI apoptosis kit. By using flow cytometry and JC-1 probe, the mitochondrial membrane potential of cells following treatment with IFN-λ1 was also examined. Expression levels of representative apoptosis‑related proteins were evaluated by western blot analysis. IFN-λ1 inhibited the proliferation of gastric carcinoma cells in a concentration‑dependent manner. IFN-λ1 increased the accumulation of cells in the sub-G0 phase and arrested the cells in the G1 phase. Exposure to IFN‑λ1 decreased the mitochondrial membrane potential and increased apoptosis. Moreover, IFN‑λ1 exposure upregulated the expression of p21, p27 and Bax, downregulated the expression of Bcl‑2, increased the release of cytochrome c and apoptosis-inducing factor (AIF) and activated caspase-3 and caspase-9. In conclusion, IFN-λ1 inhibits the proliferation of gastric carcinoma cells by arresting the cells in the G1 phase and by inducing mitochondrial‑mediated apoptosis.

Why it matters

OpenAlex reports 13 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

The aim of the present study was to examine the potential antitumor action of IFN-λ1 in human gastric carcinoma cell lines and the possible interaction between IFN-λ1 and human gastric carcinoma cells. Gastric carcinoma HGC-27 and SGC-7901 cells were treated with IFN-λ1 (0, 10, 100, 1000 ng/ml) for 48 h. Cytotoxicity was examined using an MTT method. Cell cycle distribution was examined using propidium iodide staining. Apoptosis was examined using the Annexin V-FITC/PI apoptosis kit. By using flow cytometry and JC-1 probe, the mitochondrial membrane potential of cells following treatment with IFN-λ1 was also examined. Expression levels of representative apoptosis‑related proteins were evaluated by western blot analysis. IFN-λ1 inhibited the proliferation of gastric carcinoma cells in a concentration‑dependent manner. IFN-λ1 increased the accumulation of cells in the sub-G0 phase and arrested the cells in the G1 phase. Exposure to IFN‑λ1 decreased the mitochondrial membrane potential and increased apoptosis. Moreover, IFN‑λ1 exposure upregulated the expression of p21, p27 and Bax, downregulated the expression of Bcl‑2, increased the release of cytochrome c and apoptosis-inducing factor (AIF) and activated caspase-3 and caspase-9. In conclusion, IFN-λ1 inhibits the proliferation of gastric carcinoma cells by arresting the cells in the G1 phase and by inducing mitochondrial‑mediated apoptosis.

Key concepts: Apoptosis, Propidium iodide, Cell cycle, Biology, Flow cytometry, Annexin, Molecular biology, MTT assay

Related papers

Back to paper searchBrowse research topicsOriginal source
Interferon-λ1 induces G1 phase cell cycle arrest and apoptosis in gastric carcinoma cells in vitro — Research Paper | ScholarLens