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Analysis of SCAP N-glycosylation and Trafficking in Human Cells

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ARL5B Drives Esophageal Squamous Cell Carcinoma Progression via ROCK1-SREBP1-Mediated Lipid Metabolic Reprogramming.

Xinyue Ma¹, Yanfei Sun^2,3, Hongyuan Mao¹

¹Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|October 27, 2025

Summary

Adenosine diphosphate (ADP)-ribosylation factor-like protein 5B (ARL5B) drives esophageal cancer progression by altering lipid metabolism. Inhibiting ARL5B or its associated pathway offers a potential therapeutic strategy for this aggressive malignancy.

Keywords:

ARL5B ESCC ROCK1 SREBP1 lipid metabolism

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Published on: July 21, 2018

Area of Science:

Oncology
Molecular Biology
Cancer Metabolism

Background:

Esophageal squamous cell carcinoma (ESCC) is a deadly cancer with poor survival rates.
Targeted therapies are urgently needed for effective treatment.

Purpose of the Study:

Identify novel oncogenes driving ESCC.
Elucidate the mechanism of ARL5B in ESCC progression.
Explore ARL5B as a therapeutic target.

Main Methods:

Pan-cancer analysis using The Cancer Genome Atlas (TCGA).
In vitro and in vivo functional assays (cell proliferation, invasion, apoptosis, tumor growth).
Mechanistic studies involving the ROCK1-SREBP1 signaling axis.
Pharmacological inhibition of ROCK1 and SREBP1.

Main Results:

ARL5B is upregulated in ESCC and correlates with advanced TNM stages and poor survival.
ARL5B knockdown inhibits ESCC cell proliferation, invasion, and tumor growth while promoting apoptosis.
ARL5B activates SREBP1 nuclear translocation via ROCK1, enhancing lipogenesis.
Inhibition of ROCK1 or SREBP1 reverses ARL5B-induced oncogenic effects.

Conclusions:

ARL5B is a key oncogene in ESCC, regulating lipid metabolism through the ROCK1-SREBP1 pathway.
ARL5B represents a promising therapeutic target for precision oncology in ESCC.