Page 215 - 2025中醫藥與天然藥物聯合學術研討會-中醫藥與天然藥物的挑戰Ｘ機遇與未來大會手冊

PP-33

Platycodin grandiflorum-derived exosome-like nanovesicles suppress

colorectal cancer growth by inducing cell cycle arrest through c-Myc

inhibition

1,2
1,2
1,2
1,2
Hyunyoung Choi, #,1,2 Mina Boo, Suhyeon An, HyunSoo Yang, Jae Heon Sim,
2
Dong-Hyun Youn, Hye-Lin Kim, Jinbong Park* ,2
2

1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul,
Republic of Korea
2 Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul,
Republic of Korea
*E-mail: thejinbing@khu.ac.kr

Abstract
Colorectal cancer (CRC) is a type of cancer that affects the colon or rectum, and the third
most common cancer worldwide with over 1.9 million cases diagnosed in 2022. It is also the
second leading cause of cancer-related deaths. Platycodon grandiflorum, a medicinal herb rich
of active saponins (platycodins) exhibiting therapeutic effects against cancer, obesity, and
inflammation. Despite its numerous advantages, low bioavailability, and insufficient studies on
dosage and toxicity limits its usage. In line, we herein propose Platycodin grandiflorum-derived
exosome-like nanovesicles (PELNs) as a promising delivery system with improved
bioavailability and tumor-specific anticancer effects. In this study, we investigated the pro-
apoptotic effect of PELNs in CRC cells, mediated through the induction of cell cycle arrest.
Treatment with PELNs to CT26 and HCT116 cells regulated the expression of c-Myc, a gene
frequently overexpressed in CRC and a significant factor in its progression. Specifically, we
confirmed that PELNs induced G1/S phase arrest and ultimately promoted apoptosis in colon
cancer cell lines. Based on this mechanism, we further validated the anti-cancer effects of
PELNs in an in vivo HCT116 xenograft model, without any notable toxicity. Collectively, our
findings suggest that PELNs represent a potential therapeutic agent for CRC.

Keywords: Platycodon grandiflorum-derived exosome-like nanovesicles; Colorectal cancer;
Apoptosis; c-Myc