C118P Suppresses Gastric Cancer Growth by Promoting Autophagy–Lysosomal Degradation of RAB1A
Author Information
Author(s): Wei Shihui, Zhang Jing, Wu Hai, Liao Zhengguang, Liu Zhengrui, Hou Yuhang, Du Danyu, Jiang Jingwei, Sun Li, Yuan Shengtao, Yang Mei
Primary Institution: New Drug Screening and Pharmacodynamics Evaluation Center, National Key Laboratory for Multi-Target Natural Drugs, China Pharmaceutical University, Nanjing 210009, China
Hypothesis
This study aimed to explore the anti-tumor effect of C118P against gastric cancer and identify its potential target.
Conclusion
C118P inhibits gastric cancer growth by promoting the autophagy–lysosomal-dependent degradation of RAB1A and modulating mTOR C1 signaling.
Supporting Evidence
- C118P significantly decreased the cell viability of HGC-27 and SGC-7901 cells.
- C118P induced G2/M cell cycle arrest and triggered apoptosis in gastric cancer cell lines.
- C118P was demonstrated to bind with RAB1A and reduce its protein level.
- C118P inhibited the mTORC1 signaling pathway.
- C118P treatment increased the expression of autophagy markers and promoted autophagosome formation.
Takeaway
C118P is a new drug that helps stop stomach cancer by making cancer cells break down a protein called RAB1A.
Methodology
The study used various assays including MTT, colony formation, EdU incorporation, flow cytometry, molecular docking, MST analysis, and CETSA to evaluate the effects of C118P on gastric cancer cells.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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