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A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells
Published on: July 3, 2013
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Flipping a citrate switch on liver cancer cells
1From the Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802 jmp21@psu.edu.
The Journal of Biological Chemistry
|August 20, 2017
Summary
Loss of citrate transporter solute carrier family 13 member 5 halts liver cancer cell growth. This occurs by altering energy production and mTOR signaling, suggesting a new target for liver cancer treatment.
Area of Science:
- Oncology
- Cell Biology
- Metabolism
Background:
- Energy homeostasis and oncogenic signaling are crucial for human liver cancer cell proliferation.
- Understanding the regulatory mechanisms governing these processes is vital for developing effective cancer therapies.
Purpose of the Study:
- To investigate the role of solute carrier family 13 member 5 (SLC13A5) in regulating liver cancer cell growth.
- To determine how SLC13A5 affects energy production and mammalian target of rapamycin (mTOR) signaling in liver cancer.
Main Methods:
- Utilized human liver cancer cell lines for in vitro studies.
- Employed an in vivo model of liver tumors to assess the effects of SLC13A5 loss.
- Analyzed alterations in energy production and mTOR signaling pathways.
Main Results:
- Loss of SLC13A5, a citrate transporter, significantly inhibited liver cancer cell growth.
- Disruption of SLC13A5 function altered cellular energy production.
- mTOR signaling pathways were modulated following the loss of SLC13A5.
Conclusions:
- SLC13A5 plays a critical role in maintaining liver cancer cell growth by influencing energy metabolism and mTOR signaling.
- Targeting SLC13A5 presents a potential therapeutic strategy for liver cancer chemoprevention and chemotherapy.
