The First School of Clinical Medicine, Ningxia Medical University, Yinchuan, PR China.
The First School of Clinical Medicine, Lanzhou University, Lanzhou, PR China; Department of Surgical Oncology, Gansu Provincial Hospital, Lanzhou, PR China.
Pathol Res Pract. 2024 Sep;261:155471. doi: 10.1016/j.prp.2024.155471. Epub 2024 Jul 20.
Microtubule affinity regulating kinase 4 (MARK4), which is overexpressed in various tumors, is involved in the regulation of cell division, proliferation, migration, and the cell cycle, and has been considered a potential marker for cancer; however, its mechanism of action in gastric cancer (GC) remains unclear. This study aimed to investigate the role of MARK4 in the proliferation, migration, and invasion of GC cell through the MAPK/ERK signaling pathway by targeting MARK4 knockdown.
Using The Cancer Genome Atlas data and clinical information, MARK4 expression and its relationship with prognosis were analyzed. Possible pathways involving MARK4 were explored using enrichment analysis. Western blotting and real-time quantitative polymerase chain reaction were used to detect MARK4 expression in GC. After targeted transfection of siRNA, the transfection efficiency of the experimental group was detected in AGS and HGC-27 cells. The effects of knockdown MARK4 on the proliferation, migration, and invasion of GC cells were verified using CCK-8, colony formation, wound healing, and transwell assays. Finally, the relationship between MARK4, the MAPK/ERK pathway, and epithelial-mesenchymal transition in GC was verified by western blotting.
MARK4 expression was upregulated in GC and associated with poor prognosis in patients with GC. Enrichment analysis showed that MARK4 was involved in the activation of the MAPK signaling pathway. Western blotting results indicated that MARK4 overexpression promoted the proliferation, migration, and invasion of GC cells through the MAPK/ERK pathway.
MARK4 expression was upregulated in GC and promoted the proliferation, migration, and invasion of GC cells through the MAPK/ERK pathway.
微管亲和调节激酶 4（MARK4）在多种肿瘤中过度表达，参与细胞分裂、增殖、迁移和细胞周期的调节，被认为是癌症的潜在标志物；然而，其在胃癌（GC）中的作用机制尚不清楚。本研究旨在通过靶向 MARK4 敲低，探讨 MARK4 通过 MAPK/ERK 信号通路在 GC 细胞增殖、迁移和侵袭中的作用。
利用癌症基因组图谱数据和临床信息，分析 MARK4 表达及其与预后的关系。采用富集分析探讨可能涉及 MARK4 的途径。Western blot 和实时定量聚合酶链反应检测 GC 中 MARK4 的表达。AGS 和 HGC-27 细胞经靶向转染 siRNA 后，检测实验组的转染效率。采用 CCK-8、集落形成、划痕愈合和 Transwell 实验验证敲低 MARK4 对 GC 细胞增殖、迁移和侵袭的影响。最后，通过 Western blot 验证 GC 中 MARK4、MAPK/ERK 通路和上皮-间充质转化之间的关系。
MARK4 在 GC 中表达上调，与 GC 患者的预后不良相关。富集分析显示，MARK4 参与 MAPK 信号通路的激活。Western blot 结果表明，MARK4 过表达通过 MAPK/ERK 通路促进 GC 细胞的增殖、迁移和侵袭。
MARK4 在 GC 中表达上调，通过 MAPK/ERK 通路促进 GC 细胞的增殖、迁移和侵袭。
