Follistatin‑like protein 1 knockdown elicits human gastric cancer cell apoptosis via a STAT6‑dependent pathway.

Gastric cancer is an aggressive disease and a common cause of cancer‑associated mortality worldwide. Recent studies have indicated that follistatin‑like protein 1 (FSTL‑1) is expressed and serves essential roles in tumorigenesis; however, the specific functional mechanism of FSTL‑1 in gastric cancer progression remains ambiguous. CellTiter‑Glo Luminescent Cell Viability and lactate dehydrogenase assays were used to measure cell survival and cell cytotoxicity, respectively. Cell apoptosis was ascertained using the Cell Death Detection ELISA assay and caspase‑3/9 activity kits. Reverse transcription‑quantitative polymerase chain reaction and western blotting were used to detect the expression levels of FSTL‑1. The present study confirmed that FSTL‑1 was highly expressed in gastric cancer cells compared with in control cells. Subsequently, FSTL‑1 inhibition by small interfering RNA significantly reduced cancer cell survival and induced cytotoxic effects. In addition, knockdown of FSTL‑1 in gastric cancer cells promoted apoptosis by increasing caspase‑3 and caspase‑9 expression. A decrease in signal transducer and activator of transcription 6 (STAT6) phosphorylation was observed in FSTL‑1 knockdown cells, and the results confirmed that STAT6 phosphorylation was essential for FSTL‑1 knockdown‑induced cell apoptosis of cancer cells. Taken together, these results demonstrated that FSTL‑1 knockdown may promote cell apoptosis via the STAT6 signaling pathway; therefore, FSTL1 may be considered a novel diagnostic and therapeutic target for gastric cancer.