PRELP 通过与整合素 α5 结合,降低细胞硬度和粘附性,促进结直肠癌细胞的生长和转移。

IF 3.5 3区 生物学 Q3 CELL BIOLOGY Experimental cell research Pub Date : 2024-08-01 Epub Date: 2024-07-09 DOI:10.1016/j.yexcr.2024.114151
Yajun Gui , Xiangying Deng , Namei Li , Lin Zhao
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引用次数: 0

摘要

PRELP 被认为是多种恶性肿瘤发生和发展的抑制剂。转移是结直肠癌患者死亡的主要原因,但 PRELP 在结直肠癌转移中的作用机制仍不甚明了。本研究发现,PRELP 在结直肠癌转移组织中的含量明显高于非转移组织,并且与结直肠癌患者的不良预后密切相关。PRELP促进结直肠癌细胞的生长和转移。PRELP 可降低细胞硬度和粘附性。PRELP促进结直肠癌细胞的EMT,PRELP与整合素α5结合激活整合素α5/FAK/AKT信号通路。总之,我们证明了 PRELP 在转移性结直肠癌中的上调,从生物力学的角度为转移性结直肠癌的临床治疗提供了一个潜在的预后标志物和治疗靶点。
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PRELP reduce cell stiffness and adhesion to promote the growth and metastasis of colorectal cancer cells by binding to integrin α5

PRELP is thought to be an inhibitor of the development and progression of a variety of malignancies. Metastasis is a major cause of death in patients with colorectal cancer, but the mechanism underlying the role of PRELP in colorectal cancer metastasis remains poorly understood. In this study, we found that PRELP was significantly higher in metastatic tissues than in non-metastatic tissues of colorectal cancer and was closely associated with poor prognosis of colorectal cancer patients. PRELP promotes growth and metastasis of colorectal cancer cells. PRELP reduces cell stiffness and adhesion. PRELP promoted EMT in colorectal cancer cells and that PRELP bind to integrin α5 to activate the integrin α5/FAK/AKT signaling pathway. In conclusion, we demonstrate that PRELP is upregulated in metastatic colorectal cancer, providing a potential prognostic marker and therapeutic target for the clinical management of metastatic colorectal cancer from a biomechanical perspective.

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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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