Peroxisome proliferator‐activated receptor γ coactivator 1α (PGC‐1α) is a transcriptional coactivator that has been characterized as master regulators of mitochondrial biogenesis. It has been reported that aberrant regulation of PGC‐1α is involved in a variety of human cancers. However, whether PGC‐1α is involved in the regulation of tumor growth and metastasis in gastric cancer (GC) remains unknown. In the present study, we found that the expression of PGC‐1α was upregulated in GC tissues and GC cell lines. Inhibition of PGC‐1α inhibited cell viability, migration, and invasion, and promoted cell apoptosis of GC cells. Furthermore, inhibition of PGC‐1α downregulated the SNAI1 expression, whereas upregulated microRNA (miR)‐128b expression. The expression of SNAI1 was upregulated and the expression of miR‐128b was downregulated in GC tissues. We further found that there was a positive correlation between PGC‐1α and SNAI1 expression, and a negative correlation between PGC‐1α and miR‐128b expression or between SNAI1 and miR‐128b expression in GC tissues. Moreover, PGC‐1α inhibition‐induced increased miR‐128b expression, and PGC‐1α overexpression‐induced decreased miR‐128b expression were both markedly suppressed by SNAI1 overexpression. In addition, SNAI1 overexpression or miR‐128b inhibition partly reversed the effects of PGC‐1α inhibition in GC cells. Furthermore, inhibition of PGC‐1α suppressed the tumor growth in a nude mouse model, which may be related with the dysregulation of SNAI1 and miR‐128b. In conclusion, these data indicate that the PGC‐1α/SNAI1/miR‐128b axis plays a vital role in GC via regulating cell viability, migration, invasion, and apoptosis.