[miR-155/BACH1 Signaling Pathway in Human Lung Adenocarcinoma Cell Death Induced by Arsenic Trioxide].

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.

[Effect of Cell Autophagy on the Apoptosis of Hepatocellular Carcinoma Cells Induced by Arsenic Trioxide].

Objectives: To determine the effect of autophagy on the apoptosis of hepatocellular carcinoma cells induced by arsenic trioxide (ATO).

Methods: Hepatocellular carcinoma HepG2 cells were exposed to ATO. The cell viability was detected by MTT after adjustments for autophagy agonist (Rap) and autophagy inhibitor (3-MA).

[The Experiment Study and Mechanism of Aspirin Enhances Cellular Sensitivity of Hepatocellular Carcinoma Cell Line to Arsenic Trioxide].

Objective: To explore whether aspirin could sensitize arsenic trioxide on human hepatocelluar carcinoma cell line and understanding the combination mechanisms underlying co-treatment.

Methods: Cell viability was detected by MTT assay, cell apoptosis rate and reactive oxygen species (ROS) level were measured by flow cytometry, and Western blot assay was used to estimated the protein expression of heme oxygenase-1 (HO-1) in total protein and NF-E2-related factor 2 (Nrf2) in nuclear protein.

Results: 10 μmol/L arsenic trioxide can decreased the cell viability, while cell apoptosis rate, ROS level, HO-1 and Nrf2 protein expression was increased (P < 0.