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[miR-155/BACH1 Signaling Pathway in Human Lung Adenocarcinoma Cell Death Induced by Arsenic Trioxide]
Shi-Yan Gu1, Hong-Yu Chen1, Huang-Mei Dai1
1Department of Enviromental Health and Occupational Medicine,West China School of Public Health,Sichuan University,Chengdu 610041,China.
Objective:
To explore the changes of micro RNA 155 (miR-155),BTB and CNC homologous protein 1 (BACH1),quinone oxidoreductase 1 (NQO1) and heme-oxygenase-1 (HO-1) in the process of arsenic trioxide-induced cell death,and to clarify the relationship between miR-155 and BACH1,providing experimental basis for the sensitivity of arsenic trioxide (ATO) treatment.
Methods:
Human lung adenocarcinoma cell line A549 cells were treated with different concentrations of ATO. MTT assay and total antioxidant capacity detection kit were used to determine cell viability and total antioxidant capacity,respectively. BACH1,NQO1 and HO-1 protein expression were probed by Western blot and real-time fluorescence quantitative (qRT-PCR) was utilized to test the miR-155 level. A549 cells were transfected with miR-155 mimic and its negative control,then the expression level of miR-155 was detected by qRT-PCR,and these cells were treated with 20 μmol/L for 24 h followed by MTT and Western blot detection.
Results:
10 μmol/L ATO significantly reduced the cell viability in A549 cells. 10 μmol/L and 20 μmol/L ATO treatment activated BACH1 expression and inhibited miR-155,NQO1 and HO-1 expression,leading to decreased total antioxidant capacity. Importantly,the cell death induced by 20 μmol/L ATO was significantly decreased in miR-155 mimic transfection cells in comparison with non-transfected cells and miR-155 mimic negative control transfected cells. Moreover,high expression of miR-155 reduced BACH1 activation and increased NQO1 and HO-1 expression in cells treated with 20 μmol/L ATO ( P<0.05).
Conclusion:
Restraining total antioxidant capacity contributes to ATO induced cell death,the underlying mechanisms may be that ATO can activate BACH1 expression through inhibition of the miR-155 level,leading to subsequent inhibition of NQO1 and HO-1 expression. Taken together,these data suggest that miR-155 and BACH1 could be used as sensitivity targets for ATO treatment in lung cancer.
Insights
Arsenic trioxide (ATO) induces lung cancer cell death by reducing antioxidant capacity, mediated by inhibiting micro RNA 155 (miR-155) and activating BTB and CNC homologous protein 1 (BACH1). Upregulating miR-155 may enhance ATO sensitivity.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Arsenic trioxide (ATO) is a chemotherapeutic agent.
- Lung adenocarcinoma is a major type of lung cancer.
- MicroRNAs (miRNAs) play crucial roles in cancer development and treatment response.
Purpose of the Study:
- To investigate the role of micro RNA 155 (miR-155), BTB and CNC homologous protein 1 (BACH1), quinone oxidoreductase 1 (NQO1), and heme-oxygenase-1 (HO-1) in ATO-induced cell death.
- To elucidate the relationship between miR-155 and BACH1.
- To provide a basis for improving ATO treatment sensitivity in lung cancer.
Main Methods:
- Human lung adenocarcinoma A549 cells were treated with varying concentrations of ATO.
- Cell viability and total antioxidant capacity were assessed using MTT assay and a detection kit.
- Protein expression of BACH1, NQO1, and HO-1 was analyzed by Western blot.
- miR-155 levels were quantified using real-time fluorescence quantitative PCR (qRT-PCR).
- Cells were transfected with miR-155 mimic to evaluate its effect on ATO-induced cell death and molecular changes.
Main Results:
- ATO treatment (10 μmol/L) significantly reduced A549 cell viability.
- ATO (10 and 20 μmol/L) increased BACH1 expression while decreasing miR-155, NQO1, and HO-1 levels, leading to reduced antioxidant capacity.
- Overexpression of miR-155 via transfection significantly decreased ATO-induced cell death.
- High miR-155 levels reduced BACH1 activation and increased NQO1 and HO-1 expression in ATO-treated cells (P<0.05).
Conclusions:
- Inhibition of total antioxidant capacity is crucial for ATO-induced cell death.
- ATO may activate BACH1 by suppressing miR-155, subsequently inhibiting NQO1 and HO-1.
- miR-155 and BACH1 represent potential therapeutic targets to enhance ATO sensitivity in lung cancer treatment.
