Lung cancer has become one of the leading causes of cancer-related deaths worldwide, with the most common
being non-small cell lung cancer (NSCLC). The current treatment for lung cancer is mainly chemotherapy, but
chemotherapeutic drugs generally suffer from severe side effects. Therefore, it is important to find anti-NSCLC
drugs that are safe, effective, and with few side effects. Ginsenoside compound K (CK) has not been intensively
researched for its potential as a non-toxic therapeutic medication candidate for different kinds of tumors. The
effects and functional mechanisms of CK on NSCLC are unknown. We studied the effect and involved mechanism
of CK against NSCLC in vitro and in vivo in this work. First, the MTT experiment, colony formation assay, and
cell cycle analysis all demonstrated that CK efficiently suppressed cell proliferation and induced cell cycle arrest.
Moreover, Annexin V/PI staining, JC-10 staining, ROS overproduction, western blot, immunofluorescence
staining, and TUNEL staining all showed that CK induced apoptosis. Furthermore, this study has shown that CK
inhibited the phosphorylation of EGFR, which regulates cancer cell proliferation and apoptosis by mediating
downstream PI3K/AKT/mTOR pathway. In addition, ginsenoside CK treatment dramatically suppressed tumor
growth in the xenograft nude mice model and caused no injuries. Our study established the anticancer efficacy and
mechanism of CK on NSCLC in vitro and in vivo for the first time, giving basic data supporting CK as a viable
therapy for NSCLC.
