Musk ketone induces apoptosis of gastric cancer cells via downregulation of sorbin and SH3 domain containing 2

Abstract

Musk ketone exerts antiproliferative effects on several types of cancer, such as lung and breast cancer. However, the effects and underlying mechanisms of action of musk ketone in gastric cancer (GC) are poorly understood. The present study aimed to investigate the effects of musk ketone in GC cells. The present study indicated that musk ketone exerted significant anticancer effects on GC cells. The IC 50 values of musk ketone were 4.2 and 10.06 µM in AGS and HGC-27 cells, respectively. Low dosage of musk ketone significantly suppressed the proliferation and colony formation of AGS and HGC-27 cells. Cell cycle arrest and apoptosis were induced by musk ketone. Furthermore, microarray data indicated that musk ketone treatment led to downregulation of various genes, including sorbin and SH3 domain containing 2 (SORBS2). Reverse transcription-quantitative PCR and immunoblotting results indicated that musk ketone repressed mRNA and protein expression levels of SORBS2. It was also shown that knockdown of SORBS2 inhibited the proliferation and colony formation of HGC-27 cells. The antiproliferative effects of musk ketone were decreased in HGC-27 cells with SORBS2 silencing. In summary, the present study indicated that musk ketone suppressed the proliferation and growth of GC partly by downregulating SORBS2 expression.

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“…Gastric cancer (GC) is the 4th most common malignant disease and the 2nd leading cause of cancer-associated mortality globally. 1,2 Approximately 850 000 newly diagnosed cases and 650 000 deaths occur per year. 3 What is worse, the mortality of GC ranks third among all tumors in China.…”