GINSENOSIDE CK INHIBITS THE GROWTH OF NON-SMALL CELL LUNG CANCER AND INDUCES APOPTOSIS THROUGH THE EGFR/MTOR PATHWAY IN VITRO AND IN VIVO

Paison Faida*, Linlin Qu, Jing Zhao, Xiaoxuan Ma, Rong Huang and Daidi Fan*

ABSTRACT

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.

Keywords: Anti-lung cancer effect, Apoptosis, EGFR signaling pathway, Ginsenoside CK, G1 phase arrest, Xenograft model.