Page 262 - 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-79

Antcin K inhibit cell migration and invasion in non-small cell lung cancer

cells

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Ming-Lung Hsu, Po-Chun Chen*

1 School of Life Science, National Taiwan Normal University, Taipei city, Taiwan
* E-mail: pcchen@ntnu.edu.tw

Abstract
Non-small-cell lung cancer (NSCLC) is the most prevalent form of lung cancer and
represents the leading cause of cancer-related deaths worldwide. The degradation of the
extracellular matrix (ECM) facilitates tumor invasion into surrounding tissues and distant
organs, largely through the upregulated expression of matrix metalloproteinases (MMPs).
Secreted MMPs disrupt the structural integrity of the ECM, thereby promoting tumor cell
migration and invasion. Consequently, MMPs play a critical role in driving the invasion process
during cancer progression. Antrodia cinnamomea, a medicinal fungus endemic to Taiwan, has
attracted attention for its diverse biological activities. Antcin K, an ergostane-type triterpenoid
from Antrodia cinnamomea, exhibits anti-tumor, anti-inflammatory, and immunomodulatory
activities. It has been shown to induce cancer cell apoptosis and suppress cancer cell migration
and invasion.However, The anti-metastatic effect of Antcin K on lung cancer remains to be
elucidated. In this study, we investigate the anti-metastasis effect of Antcin K in NSCLC cell
lines. We found that Antcin K significant inhibit cell migration and invasion in a dose-dependent
manner. MMP1 was identified as a target of Antcin K by using Swiss Target Prediction.
Molecular docking revealed that Antcin K may interact with MMP1. Notably, elevated MMP1
expression is significantly associated with poor overall survival in lung cancer patients. In
conclusion, Antcin K, a bioactive compound derived from Antrodia camphorata, inhibits the
migratory and invasive abilities of NSCLC cells. These findings suggest that Antcin K may
serve as a promising therapeutic candidate for preventing or limiting lung cancer metastasis.

Keywords: Antcin K; Cell migration; Cell invasion; NSCLC