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Updated: Jul 23, 2025

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
Published on: December 22, 2020
Rab11-FIP4 interacts with ARF5 to promote cancer stemness in hepatocellular carcinoma
Feifeng Song1,2, Qi Zhang1, Xixuan Lu1
1Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, China.
Rab11-FIP4 promotes hepatocellular carcinoma (HCC) stemness and sorafenib resistance by interacting with ARF5. Targeting Rab11-FIP4 may offer a new therapeutic strategy for HCC.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Rab11-family interacting proteins (Rab11-FIPs) are implicated in tumorigenesis.
- Rab11-FIP4 is upregulated in hepatocellular carcinoma (HCC), but its role in HCC stemness is unknown.
Purpose of the Study:
- To investigate the role of Rab11-FIP4 in HCC stemness and its underlying mechanism.
- To explore Rab11-FIP4 as a potential therapeutic target for HCC.
Main Methods:
- Quantification of Rab11-FIP4 expression in HCC cell lines and tissues.
- Functional assays including sphere formation and stemness marker analysis (ALDH1A1, CD133, NANOG, OCT4).
- Investigation of the interaction between Rab11-FIP4, ARF5, and cell cycle proteins (CDK1/cyclin B).
Main Results:
- Rab11-FIP4 expression is elevated in HCC and correlates positively with cancer stemness.
- Overexpression of Rab11-FIP4 promotes sphere formation and stemness markers; knockdown suppresses CSC-like traits.
- Rab11-FIP4 knockdown enhances HCC cell sensitivity to sorafenib.
- Rab11-FIP4 interacts with ARF5, influencing CDK1/cyclin B to promote HCC stemness.
Conclusions:
- Rab11-FIP4 plays a critical role in regulating cancer stem cell (CSC)-like properties in HCC.
- Rab11-FIP4 is identified as a potential therapeutic target for hepatocellular carcinoma.
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