A 71-year-old man had undergone branched open stent grafting for a distal arch aneurysm in May 2006. He subsequently developed multiple episodes of postoperative endoleak successfully treated by TEVAR in January and November 2009. He visited our hospital complaining of back pain in May 2011. Chest computed tomography showed increasing size of the aneurysm and recurrent endoleak of the distal stent graft, and impending rupture of the aneurysm was diagnosed. Considering the technical difficulty of repair by TEVAR, we performed graft replacement of the aneurysm with removal of the previous stent graft. The postoperative course was unremarkable and he was discharged on postoperative day 11.

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