Cambridge-Suda (CAM-SU) Genome Resource Center, Soochow University, and Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou 215123, China.
Department of Pathology, The Third Affiliated Hospital of Soochow University, Changzhou 213004, China.
Biomed Pharmacother. 2017 Aug;92:810-818. doi: 10.1016/j.biopha.2017.05.139. Epub 2017 Jun 10.
Leiomyosarcoma is a rare malignant smooth muscle tumor which can be very unpredictable. Myosin II is involved in many functions, including cell contraction, migration, and adhesion. The phosphorylation of myosin regulatory light chain (MLC) by myosin light chain kinase (MLCK) determines the activity of Myosin II. However, it is still unclear whether MLC phosphorylation is involved in cell proliferation in leiomyosarcoma. In this study, we aimed to explore the role of MLCK-dependent MLC phosphorylation in leiomyosarcoma development. We found that the expression of MLCK, phosphorylated MLC, and Ki67 in leiomyosarcoma was significantly higher than in leiomyoma and adjacent normal smooth muscle cells. MLCK expression was significantly correlated with phosphorylated MLC level. Kaplan-Meier survival analysis revealed that patients with high expression of MLCK or phosphorylated MLC had shorter overall survival times compared with the patients with low expression of MLCK or phosphorylated MLC. In vitro studies revealed a causative link between MLC phosphorylation and cellular proliferation as expression of phosphomimetic MLC (T19D, S20D) increased cellular proliferation as assessed by Ki67 staining. In contrast, MLCK specific inhibitor reduced cellular proliferation. We concluded that MLCK, phosphorylated MLC and Ki67 were overexpressed in leiomyosarcoma. MLCK dependent MLC phosphorylation might be responsible for the high proliferative state in leiomyosarcoma. MLCK and phosphorylated MLC are potential prognostic indicators of leiomyosarcoma.
平滑肌肉瘤是一种罕见的恶性平滑肌肿瘤,其行为难以预测。肌球蛋白 II 参与许多功能,包括细胞收缩、迁移和黏附。肌球蛋白轻链激酶(MLCK)使肌球蛋白调节轻链(MLC)磷酸化,决定肌球蛋白 II 的活性。然而,MLC 磷酸化是否参与平滑肌肉瘤细胞增殖仍不清楚。本研究旨在探讨 MLCK 依赖性 MLC 磷酸化在平滑肌肉瘤发生发展中的作用。我们发现,平滑肌肉瘤中 MLCK、磷酸化 MLC 和 Ki67 的表达明显高于平滑肌瘤和相邻正常平滑肌细胞。MLCK 表达与磷酸化 MLC 水平显著相关。Kaplan-Meier 生存分析显示,MLCK 或磷酸化 MLC 高表达的患者总生存时间明显短于 MLCK 或磷酸化 MLC 低表达的患者。体外研究显示 MLC 磷酸化与细胞增殖之间存在因果关系,因为磷酸化 MLC(T19D、S20D)的表达增加,Ki67 染色评估的细胞增殖增加。相反,MLCK 特异性抑制剂减少了细胞增殖。我们得出结论,MLCK、磷酸化 MLC 和 Ki67 在平滑肌肉瘤中过度表达。MLCK 依赖性 MLC 磷酸化可能是平滑肌肉瘤高增殖状态的原因。MLCK 和磷酸化 MLC 是平滑肌肉瘤的潜在预后指标。