SK4 oncochannels regulate calcium entry and promote cell migration in KRAS-mutated colorectal cancer.
作者： William Raoul , Maxime Guéguinou , Thierry Lecomte , Yann Fourbon , Laetitia Corset
DOI: 10.1016/J.CECA.2021.102384
关键词: Intracellular 、 KRAS 、 Cancer research 、 Potassium channel 、 Calcium signaling 、 Metastasis 、 Colorectal cancer 、 Cell migration 、 KCNN4 、 Chemistry
摘要: Abstract Background Colorectal cancer (CRC) metastases are the main cause of CRC mortality. Intracellular Ca2+ regulates cell migration and invasion, key factors for metastases. also activates Ca2+-dependent potassium channels which in turn affect driving force. We have previously reported that expression activated channel KCNN4 (SK4) is higher primary tumors compared to normal tissues. Here, we aimed investigate role SK4 physiology CRC. Results protein enhanced tissues colon tissues, with a level patients KRAS mutations. At cellular level, found membrane potential HCT116 cells. its inhibition reduced store operated entry (SOCE) constitutive (CCE), while reducing migration. activity linked resistance pathways such as mutation NRF2 HIF-1α. In addition, pharmacological intracellular reactive oxygen species (ROS) production, HIF1α stabilization. Conclusion Our results suggest contributes colorectal invasion by modulating both ROS regulation. Therefore, could be target reduce metastasis KRAS-mutated
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