Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang 330031, China.
Department of Gastrointestinal Surgery, The First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning, 530021 Guangxi Zhuang Autonomous Region, China.
Oxid Med Cell Longev. 2022 Sep 24;2022:8611306. doi: 10.1155/2022/8611306. eCollection 2022.
ITGA5 is an adhesion molecule that integrates the intracellular structures with the extracellular matrix to perform biological functions. However, ITGA5 is highly expressed in a variety of tumors and is involved in tumor progression by promoting cell proliferation and metastasis. Nevertheless, little research has been performed on its function in gastric cancer. Therefore, the aim of this study was to investigate the role of ITGA5 in gastric cancer, focusing on the mechanism regulating the proliferation, invasion and migration.
The expression of ITGA5 in gastric cancer tissues was assessed by the use of molecular bioinformatics databases and high-throughput sequencing of gastric cancer tissues from patients. Western blot, qPCR, and immunohistochemistry were performed to detect the expression of ITGA5 in samples from gastric cancer patients and gastric cancer cell lines. Furthermore, the ITGA5 gene was silenced and overexpressed in gastric cancer cells, and the effect on proliferation, invasion, migration, and tumorigenic ability was assessed.
ITGA5 mRNA and protein expression were upregulated in gastric cancer cell lines and tissues from patients, and its expression was closely associated with tumor size, lymph node metastasis, and TNM stage. and experiments showed that ITGA5 silencing resulted in the inhibition of proliferation, invasion, migration, and graft growth of gastric cancer cells; conversely, the overexpression resulted in the promotion of these cell functions. Our results finally showed that the effect of ITGA5 on proliferation, invasion, and migration of gastric cancer cells was performed through the activation of the FAK/AKT pathway.
ITGA5 promotes proliferation, invasion, and migration of gastric cancer cells through the activation of FAK/AKT signaling pathway, suggesting that ITGA5 may be potentially considered as a new target in gastric cancer therapy.
ITGA5 是一种黏附分子，它将细胞内结构与细胞外基质整合在一起，以发挥生物学功能。然而，ITGA5 在多种肿瘤中高表达，并通过促进细胞增殖和转移参与肿瘤进展。尽管如此，关于其在胃癌中的功能研究甚少。因此，本研究旨在探讨 ITGA5 在胃癌中的作用，重点研究调节增殖、侵袭和迁移的机制。
使用分子生物信息学数据库和高通量测序技术评估胃癌组织中 ITGA5 的表达。通过 Western blot、qPCR 和免疫组织化学检测来自胃癌患者和胃癌细胞系的样本中 ITGA5 的表达。此外，在胃癌细胞中沉默和过表达 ITGA5 基因，并评估对增殖、侵袭、迁移和致瘤能力的影响。
ITGA5 mRNA 和蛋白表达在胃癌细胞系和患者组织中上调，其表达与肿瘤大小、淋巴结转移和 TNM 分期密切相关。体内和体外实验表明，ITGA5 沉默导致胃癌细胞增殖、侵袭、迁移和移植瘤生长受到抑制；相反，过表达促进了这些细胞功能。我们的研究结果最终表明，ITGA5 通过激活 FAK/AKT 信号通路对胃癌细胞的增殖、侵袭和迁移发挥作用。
ITGA5 通过激活 FAK/AKT 信号通路促进胃癌细胞的增殖、侵袭和迁移，表明 ITGA5 可能有望成为胃癌治疗的新靶点。
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