Abstract：
Cell metastasis is the main cause of cancer mortality. Inhibiting early events during cell metastasis and invasion could significantly improve cancer prognosis, but the initial mechanisms of cell transition and migration are barely known. Calcium regulates cell migration, whilst Thymosin β4 is a G-actin and iron binding peptide associated with tumor metastasis and ferroptosis. Under normal cell growth conditions, intracellular free calcium ions and Thymosin β4 concentrations are strictly regulated, and are not influenced by extracellular supplementation. However, cell starvation decreases intracellular Thymosin β4 and increases extracellular peptide uptake above the normal range. Unexpectedly, cell starvation significantly increases internalization of extracellular Ca2+/Thymosin β4 complexes. Elucidating the role of Ca2+/Thymosin β4 in the early events of metastasis will likely be important in the future to develop therapies targeting metastasis.
摘要：
细胞转移是癌症死亡的主要原因。抑制细胞转移和侵袭过程中的早期事件可以显着改善癌症的预后。但是细胞转移和迁移的最初机制鲜为人知。钙调节细胞迁移，而胸腺素β4是与肿瘤转移和铁凋亡相关的G-肌动蛋白和铁结合肽。在正常的细胞生长条件下，细胞内游离钙离子和胸腺肽β4浓度受到严格调控，并且不受细胞外补充的影响。然而,细胞饥饿降低细胞内胸腺肽β4并增加细胞外肽摄取高于正常范围。出乎意料的是,细胞饥饿显着增加细胞外Ca2/胸腺肽β4复合物的内化。阐明Ca2/胸腺肽β4在转移早期事件中的作用可能在将来开发靶向转移的疗法中很重要。
