Scholarlink

<p>Lidocaine is an inhibitor of voltage-gated sodium channels (VGSCs) expressed in excitable cells, such as myocardial cells and sensory neurons, and is used in many clinical situations, including as an anti-arrhythmic and analgesic agent. Clinical studies have suggested that its perioperative application in cancer patients improves their prognosis. Na<sub>v</sub>1.5 encoded by the SCN5A gene, which forms the α subunit of VGSC and is a pharmacological target of lidocaine, is expressed in various types of cancer cells. The SCN5A gene is also identified as an upstream regulator of the invasive activity of colon cancer cells, and its aberrant expression correlates with malignancy. Although we previously demonstrated that lidocaine treatment inhibits the growth of cancer cell lines, whether lidocaine induces cell growth suppression through inhibition of Na<sub>v</sub>1.5 is still unresolved. Here, we demonstrated that lidocaine induces growth suppression of colon cancer SW480 cells along with a decrease of Na<sub>v</sub>1.5. Additionally, lidocaine decreased cyclin D1, a cell cycle promoter, and mutant p53, which has transforming activity in SW480 cells. Since the expression level of Na<sub>v</sub>1.5 is associated with the invasiveness of colon cancer, the decrease of Na<sub>v</sub>1.5 with the administration of lidocaine has potential as a novel therapeutic strategy for cancer.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The local anesthetic, lidocaine, suppresses the growth of colon cancer SW480 cells by decreasing the voltage-gated sodium channel subunit Nav1.5

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月22日

查看全文
  • Keiko Haraguchi-Suzuki,
  • Toru Suzuki,
  • Chigusa Nakasone,
  • Reika Kawabata-Iwakawa,
  • Shigeru Saito

摘要

Lidocaine is an inhibitor of voltage-gated sodium channels (VGSCs) expressed in excitable cells, such as myocardial cells and sensory neurons, and is used in many clinical situations, including as an anti-arrhythmic and analgesic agent. Clinical studies have suggested that its perioperative application in cancer patients improves their prognosis. Nav1.5 encoded by the SCN5A gene, which forms the α subunit of VGSC and is a pharmacological target of lidocaine, is expressed in various types of cancer cells. The SCN5A gene is also identified as an upstream regulator of the invasive activity of colon cancer cells, and its aberrant expression correlates with malignancy. Although we previously demonstrated that lidocaine treatment inhibits the growth of cancer cell lines, whether lidocaine induces cell growth suppression through inhibition of Nav1.5 is still unresolved. Here, we demonstrated that lidocaine induces growth suppression of colon cancer SW480 cells along with a decrease of Nav1.5. Additionally, lidocaine decreased cyclin D1, a cell cycle promoter, and mutant p53, which has transforming activity in SW480 cells. Since the expression level of Nav1.5 is associated with the invasiveness of colon cancer, the decrease of Nav1.5 with the administration of lidocaine has potential as a novel therapeutic strategy for cancer.