Effect of autophagy inhibition on cell viability and cell cycle progression in MDA‑MB‑231 human breast cancer cells.

Atg7 is an autophagy‑related gene, and is involved in two ubiquitin‑like conjugation systems in the process of autophagy. It is well established that 3‑methyladenine (3Ma) is an autophagy inhibitor. The present study aimed to investigate the effect of autophagy inhibition on the cell viability and cell cycle progression of human breast cancer cells. MDA‑MB‑231 human breast cancer cells were cultured in Dulbecco's modified Eagle's medium (DMEM) with high glucose, then divided into six groups. The six groups included the three fundamental groups as follows: The control group (untreated); the starvation group (high‑glucose DMEM replaced with glucose‑free minimal essential medium); and the starvation 3Ma group (maintained in glucose‑free culture medium and treated with the autophagy inhibitor 3Ma). The three fundamental groups were further divided into Atg7 siRNA‑transfected and non‑transfected groups. The cell viability and apoptosis of each group was determined by MTT assay and flow cytometry. The results of the current study demonstrated that Atg7 deficiency alone had no statically significant effect on the cell viability of MDA‑MB‑231 human breast cancer cells, while 3Ma reduced the cell viability and its effect was potentiated by Atg7 deficiency. Atg7 deficiency was more intense than 3Ma in the promotion of apoptosis and cell arrest in G0/G1‑phase in the absence of glucose and its effect was reduced by 3Ma. In conclusion, 3Ma and Atg7 may be involved in different pathways in the process of autophagy. Inhibition of autophagy may influence the cell viability and cell cycle through different pathways in MDA‑MB‑231 human breast cancer cells.