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18P - Choline transporter-like protein 1 (CTL1/SLC44A1) is a therapeutic target molecule for prostate cancer therapy (ID 115)

Presentation Number
Lecture Time
18:25 - 18:25
  • M. Inazu
Hall Bordeaux, Palais des Congrès, Paris, France
18:00 - 18:45
  • M. Inazu
  • I. Saiki
  • H. Uchino
  • T. Yamanaka



Prostate cancer is one of the most common types of cancer in men. Choline is an essential component of cell membrane phospholipids and is metabolized and internalized into cells by choline kinase, an enzyme that is overexpressed in certain tumors, such as prostate cancer. Two choline tracers are available for clinical use, which are labeled either with 11C-choline or with 18F-choline. These choline PET tracers that target cell membrane metabolism have influenced prostate cancer imaging, particularly in biochemical relapse, and are therefore FDA approved for use in patients with recurrent disease. However, the uptake system for choline and the functional expression of choline transporters in prostate cancer are not totally understood.


We examined [3H]choline uptake in the prostate cancer cell line LNCaP, which depends on androgen. Cells were cultured in RPMI 1640 medium supplemented with 10 % fetal bovine serum and grown at 37 °C in 5% CO2. The CellTiter-Glo Luminescent Cell Viability Assay is a homogeneous method of determining the number of viable cells. The Caspase-Glo 3/7 assay reagent was used for caspase detection in treated cells.


[3H]Choline uptake is mediated by a single Na+-independent and intermediate-affinity transport system. Choline transporter-like protein 1 (CTL1) and CTL2 mRNA are highly expressed. CTL1 and CTL2 immunoreactivity were recognized in the plasma membrane and intracellular compartments, respectively. The anticancer drugs, flutamide, and bicalutamide inhibited cell viability and [3H]choline uptake in a concentration-dependent manner. The correlations between the effect of both anticancer drugs for cell viability and [3H]choline uptake were significant. The caspase-3/7 activity significantly increased by flutamide and bicalutamide. Furthermore, both flutamide and bicalutamide decreased the expression level of CTL1 in LNCaP cells.


These results suggest that CTL1 are functionally expressed in prostate cancer cells and are also involved in abnormal proliferation. Identification of this CTL1-mediated choline transport system provides a potential new target for prostate cancer therapy.

Legal entity responsible for the study

Tokyo Medical University.


Has not received any funding.


All authors have declared no conflicts of interest.