Decrease in the hip extension range of motion (HE-ROM) can cause lumbar hyperlordosis. Hyperlordosis is one of the mechanisms underlying low back pain. A diagnosis of low back pain from hyperlordosis can be used to detect the area in which hyperlordosis occurs more easily—the upper or lower lumbar spine. Twenty-one men were recruited for this study. HE-ROM was measured manually. Lumbar alignment was measured on a bed in a prone position. We extended the subject's hip by bending the bed at 4 angles (0°, 10°, 15°, 30°) and measured the spinal alignment by using a SpinalMouse. The results showed that lumbar lordosis increased at the bed angles of 15°and 30°. Only when the bed angle was changed from 0° to 30°, the increased angle of the lumbar spine was negatively correlated to the HE-ROM (r=-0.46, p<0.05), particularly that of the lower lumbar spine (r=-0.47, p<0.05). These findings suggested that lower lumbar lordosis tends to increase in individuals with poor HE-ROM. Additionally, increase in lower lumbar lordosis is attributed to the tendency to have low back pain in the lower lumbar spine.

Prostate cancer is one of the most common cancers in men. Choline PET or PET/CT has been used to visualize prostate cancer, and high levels of choline accumulation have been observed in tumors. However, the uptake system for choline and the functional expression of choline transporters in prostate cancer are not completely understood. In this study, the molecular and functional aspects of choline uptake were investigated in the LNCaP prostate cancer cell line along with the correlations between choline uptake and cell viability in drug-treated cells. Choline transporter-like protein 1 (CTL1) and CTL2 mRNA were highly expressed in LNCaP cells. CTL1 and CTL2 were located in the plasma membrane and mitochondria, respectively. [3H]Choline uptake was mediated by a single Na+-independent, intermediate-affinity transport system in the LNCaP cells. The anticancer drugs, flutamide and bicalutamide, inhibited cell viability and [3H]choline uptake in a concentration-dependent manner. The correlations between the effects of these drugs on cell viability and [3H]choline uptake were significant. Caspase-3/7 activity was significantly increased by both flutamide and bicalutamide. Furthermore, these drugs decreased CTL1 expression in the prostate cancer cell line. These results suggest that CTL1 is functionally expressed in prostate cancer cells and are also involved in abnormal proliferation. Identification of this CTL1-mediated choline transport system in prostate cancer cells provides a potential new therapeutic target for the treatment of this disease.

In this study, we examined the molecular and functional characterization of choline uptake in the human esophageal cancer cells. In addition, we examined the influence of various drugs on the transport of [3H]choline, and explored the possible correlation between the inhibition of choline uptake and apoptotic cell death. We found that both choline transporter-like protein 1 (CTL1) and CTL2 mRNAs and proteins were highly expressed in esophageal cancer cell lines (KYSE series). CTL1 and CTL2 were located in the plasma membrane and mitochondria, respectively. Choline uptake was saturable and mediated by a single transport system, which is both Na+-independent and pH-dependent. Choline uptake and cell viability were inhibited by various cationic drugs. Furthermore, a correlation analysis of the potencies of 47 drugs for the inhibition of choline uptake and cell viability showed a strong correlation. Choline uptake inhibitors and choline deficiency each inhibited cell viability and increased caspase-3/7 activity. We conclude that extracellular choline is mainly transported via a CTL1. The functional inhibition of CTL1 by cationic drugs could promote apoptotic cell death. Furthermore, CTL2 may be involved in choline uptake in mitochondria, which is the rate-limiting step in S-adenosylmethionine (SAM) synthesis and DNA methylation. Identification of this CTL1- and CTL2-mediated choline transport system provides a potential new target for esophageal cancer therapy.
Cell Death ; Cell Line ; Cell Membrane ; Cell Survival ; Choline Deficiency ; Choline* ; DNA Methylation ; Esophageal Neoplasms* ; Humans ; Mitochondria ; RNA, Messenger ; S-Adenosylmethionine