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Updated: Apr 1, 2026
A Fluorescence-based Assay for Characterization and Quantification of Lipid Droplet Formation in Human Intestinal Organoids
Published on: October 13, 2019
The lipid transfer protein STARD7 controls intestinal tumor development in a context-dependent manner
Kateryna Shostak1, Yu Chen1, Chloé Maurizy1
1Laboratory of Cancer Biology, GIGA Cancer, University of Liege, Sart-Tilman, Liège, Belgium.
Abstract:
The role of phosphatidylcholine transporters such as Stard7 in intestinal cancer development is unknown. To explore this issue, we generated a mouse model lacking Stard7 in intestinal epithelial cells (IECs). Loss of Stard7 impaired mitochondrial Complex I activity, led to a severe metabolic and lipid reprogramming, enhanced mitochondrial ROS production and potentiated an mTORC1/ATF4 signature. As a result, levels of enzymes involved in serine biosynthesis were enhanced in Stard7-deficient IECs. We next assessed the consequences of Stard7 deficiency in both Wnt-dependent tumor initiation and in inflammation-driven tumor development. Strikingly, despite generating similar molecular signatures, Stard7 deficiency inhibited tumor development in Azoxymethane (AOM)/Dextran Sulfate Sodium (DSS)-treated mice but promoted Wnt-driven cancer initiation in the intestine. Apc+/Min mice lacking Stard7 in IECs developed more tumors in the distal colon as well as a specific microbiota signature. Collectively, our results suggest that the genetic status critically controls the effects of Stard7 deficiency on intestinal tumor development.
Insights
Stard7 transporter deficiency impacts intestinal cancer by altering cell metabolism and mitochondrial function. Its effect on tumor growth depends on the genetic context, either inhibiting or promoting cancer initiation.
Area of Science:
- Molecular Biology
- Oncology
- Metabolism
Background:
- The role of phosphatidylcholine transporters, like Stard7, in intestinal cancer is not well understood.
- Stard7 is crucial for lipid transport and cellular homeostasis.
Purpose of the Study:
- To investigate the function of Stard7 in intestinal epithelial cells (IECs) in the context of cancer development.
- To determine how Stard7 deficiency affects tumor initiation and progression in different models.
Main Methods:
- Generated a mouse model with Stard7 specifically deleted in IECs.
- Utilized Wnt-driven (Apc+/Min) and inflammation-driven (AOM/DSS) intestinal cancer models.
- Analyzed metabolic reprogramming, mitochondrial function, and tumor development.
Main Results:
- Stard7 loss impaired mitochondrial Complex I, altered lipid metabolism, increased ROS, and activated mTORC1/ATF4 signaling.
- Stard7 deficiency inhibited inflammation-driven tumors but promoted Wnt-driven intestinal cancer.
- Apc+/Min mice lacking Stard7 showed increased distal colon tumors and altered microbiota.
Conclusions:
- Stard7 plays a context-dependent role in intestinal tumorigenesis.
- Genetic background critically influences the impact of Stard7 deficiency on intestinal cancer.
- Stard7 is a potential factor in modulating cancer development based on cellular environment.
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