Park Sungjin David, Saunders Apryl S, Reidy Megan A, Bender Dawn E, Clifton Shari, Morris Katherine T
Department of Surgery, University of Oklahoma Health Science Center, Oklahoma City, OK, United States.
Department of Information Management, University of Oklahoma Health Science Center, Oklahoma City, OK, United States.
Front Oncol. 2022 Aug 11;12:932608. doi: 10.3389/fonc.2022.932608. eCollection 2022.
Granulocyte colony-stimulating factor receptor (GCSFR) is a critical regulator of granulopoiesis. Studies have shown significant upregulation of GCSFR in a variety of cancers and cell types and have recognized GCSFR as a cytokine receptor capable of influencing both myeloid and non-myeloid immune cells, supporting pro-tumoral actions. This systematic review aims to summarize the available literature examining the mechanisms that control GCSFR signaling, regulation, and surface expression with emphasis on how these mechanisms may be dysregulated in cancer. Experiments with different cancer cell lines from breast cancer, bladder cancer, glioma, and neuroblastoma are used to review the biological function and underlying mechanisms of increased GCSFR expression with emphasis on actions related to tumor proliferation, migration, and metastasis, primarily acting through the JAK/STAT pathway. Evidence is also presented that demonstrates a differential physiological response to aberrant GCSFR signal transduction in different organs. The lifecycle of the receptor is also reviewed to support future work defining how this signaling axis becomes dysregulated in malignancies.
粒细胞集落刺激因子受体（GCSFR）是粒细胞生成的关键调节因子。研究表明，GCSFR在多种癌症和细胞类型中显著上调，并已被确认为一种细胞因子受体，能够影响髓系和非髓系免疫细胞，支持促肿瘤作用。本系统综述旨在总结现有文献，探讨控制GCSFR信号传导、调节和表面表达的机制，重点关注这些机制在癌症中可能如何失调。使用来自乳腺癌、膀胱癌、胶质瘤和神经母细胞瘤的不同癌细胞系进行实验，以综述GCSFR表达增加的生物学功能和潜在机制，重点关注与肿瘤增殖、迁移和转移相关的作用，主要通过JAK/STAT途径发挥作用。还提供了证据，证明不同器官对异常GCSFR信号转导有不同的生理反应。还对该受体的生命周期进行了综述，以支持未来关于确定该信号轴在恶性肿瘤中如何失调的研究工作。
