Journal of cancer research and therapeutics · 2026
A study on the antitumor effect and mechanism of arsenic trioxide on lung adenocarcinoma.
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Zheng Qixian, Liu Haiyu, Zhang Qianyuan, Guo Ningjing, Luo Qiong, Yang Sheng, Zhang Suyun, Chen Xiangqi, Li Nan
Аннотация
BACKGROUND: Lung adenocarcinoma is a common malignancy that requires new treatments. Arsenic trioxide (ATO) exerts antitumor activity in various cancers; however, its mechanisms of action in lung adenocarcinoma remain unclear.
METHODS: The 24-h half-maximal inhibitory concentration (IC50) of ATO on human lung adenocarcinoma A549 cells was determined using the Cell Counting Kit-8 assay. Cells were treated with the IC50 concentration in the experimental group, and untreated cells served as the control group. A comparative assessment of cell proliferation, apoptosis, invasion, and migration was performed. Transcriptome sequencing followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted to identify differentially expressed genes and enriched pathways. Candidate pathway proteins were validated by western blot analysis.
RESULTS: The 24-h IC50 of ATO was 99.12 μmol/L. The ATO-treated group exhibited reduced proliferation, increased apoptosis, and decreased invasion and migration ( P < 0.05) compared with that in the control group. Transcriptome analysis revealed 4,522 upregulated and 4,045 downregulated genes, with enrichment in the mammalian target of rapamycin (mTOR) signaling pathway, base excision repair (BER), and apoptosis pathways. At the protein level, total mTOR expression did not significantly change, whereas phosphorylated mTOR (p-mTOR), APE-1, Bcl-2, and Bcl-XL were downregulated, and cleaved caspase-8 and cleaved caspase-9 were upregulated ( P < 0.05).
DISCUSSION: These results indicate that ATO suppresses the malignant phenotype of A549 cells by inhibiting mTOR phosphorylation, downregulating key BER components, and activating the extrinsic and intrinsic apoptotic pathways, providing experimental evidence for further studies of ATO in lung adenocarcinoma therapy.
METHODS: The 24-h half-maximal inhibitory concentration (IC50) of ATO on human lung adenocarcinoma A549 cells was determined using the Cell Counting Kit-8 assay. Cells were treated with the IC50 concentration in the experimental group, and untreated cells served as the control group. A comparative assessment of cell proliferation, apoptosis, invasion, and migration was performed. Transcriptome sequencing followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted to identify differentially expressed genes and enriched pathways. Candidate pathway proteins were validated by western blot analysis.
RESULTS: The 24-h IC50 of ATO was 99.12 μmol/L. The ATO-treated group exhibited reduced proliferation, increased apoptosis, and decreased invasion and migration ( P < 0.05) compared with that in the control group. Transcriptome analysis revealed 4,522 upregulated and 4,045 downregulated genes, with enrichment in the mammalian target of rapamycin (mTOR) signaling pathway, base excision repair (BER), and apoptosis pathways. At the protein level, total mTOR expression did not significantly change, whereas phosphorylated mTOR (p-mTOR), APE-1, Bcl-2, and Bcl-XL were downregulated, and cleaved caspase-8 and cleaved caspase-9 were upregulated ( P < 0.05).
DISCUSSION: These results indicate that ATO suppresses the malignant phenotype of A549 cells by inhibiting mTOR phosphorylation, downregulating key BER components, and activating the extrinsic and intrinsic apoptotic pathways, providing experimental evidence for further studies of ATO in lung adenocarcinoma therapy.