肌动蛋白调节蛋白--1(Profilin--1)在胃癌中的作用及机制研究.docx

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Introduction
Gastric cancer (GC) is one of the most common gastrointestinal cancers, with high morbidity and mortality rates worldwide. Despite advances in diagnosis and treatment, the mechanisms underlying GC pathogenesis and progression remain unclear. Numerous studies have shown that abnormal cellular and molecular events, such as altered cytoskeletal dynamics, contribute to GC development. Among these, the interactions between cytoskeletal actin and its binding proteins have been implicated in the invasion and metastasis of GC. In particular, profilin-1 (Pfn-1) is a key regulator of actin dynamics and has been found to play a critical role in the development and progression of GC. In this review, we summarize the current knowledge regarding Pfn-1’s role in GC and its underlying mechanisms.
The Role of Profilin-1 in Gastric Cancer
Pfn-1 is a small, ubiquitous cytoplasmic protein that binds to actin monomers and regulates filament assembly in eukaryotic cells. In GC, Pfn-1 expression has been shown to be significantly increased compared to normal gastric tissues, and high levels of Pfn-1 correlate with more advanced tumor stages and poorer prognoses. Experimental evidence also suggests that Pfn-1 promotes GC cell migration, invasion, and metastasis by regulating actin dynamics. Furthermore, Pfn-1 has been found to interact with various signaling pathways involved in GC development and progression, including the Wnt/β-catenin, PI3K/Akt, and MAPK/ERK pathways.
Wnt/β-catenin Pathway
The Wnt/β-catenin pathway is a critical signaling pathway involved in the regulation of cell proliferation, differentiation, and migration. Wnt signaling is initiated by binding of Wnt ligands to Frizzled receptors, leading to stabilization and nuclear translocation of β-catenin and subsequent activation of Wnt target genes. Aberrant activation of the Wnt/β-catenin pathway has been implicated in many types of cancer, including GC. Recent studies have shown that Pfn-1 enhances Wnt/β-catenin signaling by interacting with various components of the pathway. For example, Pfn-1 has been found to associate with Dishevelled (Dvl), a key regulator of Wnt signaling, and to promote the formation of Dvl/Pfn-1 complexes, which enhance β-catenin stabilization and nuclear translocation. In addition, Pfn-1 has been shown to promote β-catenin-mediated transcriptional activation by interacting with T-cell factor/lymphoid enhancer factor (TCF/LEF), the main transcription factors involved in Wnt target gene expression. These findings suggest that Pfn-1 may play a role in GC by promoting Wnt/β-catenin signaling.
PI3K/Akt Pathway
The PI3K/Akt pathway is another critical signaling pathway involved in the regulation of cell growth, survival, and motility. Activation of this pathway is frequently observed in human tumors and is associated with cancer development and progression. In GC, Pfn-1 has been found to enhance PI3K/Akt signaling by regulating the activity of Akt. Specifically, Pfn-1 has been shown to interact with Akt and to promote its phosphorylation and activation. In addition, Pfn-1 has been found to regulate the subcellular localization of Akt, promoting its translocation from the cytoplasm to the plasma membrane, where it is activated by growth factors and other stimuli. These findings suggest that Pfn-1 may promote GC by enhancing PI3K/Akt signaling.
MAPK/ERK Pathway
The MAPK/ERK pathway is a family of signaling pathways involved in the regulation of cell proliferation, differentiation, survival, and motility. Dysregulation of this pathway has been implicated in various types of cancer, including GC. Pfn-1 has been found to promote MAPK/ERK activation by binding to and activating extracellular signal-regulated kinase (ERK). Specifically, Pfn-1 has been shown to bind to the ERK 2 catalytic domain, enhancing its phosphorylation and activation. Furthermore, Pfn-1 has been found to enhance the translocation of phosphorylated ERK to the nucleus, where it activates target genes involved in cell proliferation and survival. These findings suggest that Pfn-1 may promote GC by enhancing MAPK/ERK signaling.
Conclusion
In summary, Pfn-1 is a critical regulator of actin dynamics that plays a key role in GC development and progression. Pfn-1 promotes GC through various pathways, including Wnt/β-catenin, PI3K/Akt, and MAPK/ERK signaling. These findings suggest that Pfn-1 may serve as a potential therapeutic target for the treatment of GC, although further studies are needed to fully elucidate its function in this deadly disease.