Department of Gastroenterology, Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Putuo District, Shanghai, 200065, People's Republic of China.
Department of Gastroenterology, Putuo People's Hospital, Tongji University, Shanghai, 200060, People's Republic of China.
Biomed Eng Online. 2022 May 20;21(1):30. doi: 10.1186/s12938-022-00998-5.
Integrin, beta-like 1 (ITGBL1) is involved in a variety of human malignancies. However, the information on the involvement of ITGBL1 in gastric carcinoma (GC) is limited. Hence, this study aimed further to explore the functions and mechanisms of ITGBL1 in GC.
First, multiple bioinformatics databases, including Oncomine, Tumor Immune Estimation Resource, UALCAN, and Kaplan-Meier Plotter, were used to predict the expression level and prognostic value of ITGBL1, as well as its association with immune infiltration and epithelial-mesenchymal transition (EMT) in GC. Quantitative reverse transcription-polymerase chain reaction and immunohistochemical analysis were used to detect the expression of ITGBL1 in both GC tissues and cells. Then, targeted silencing of ITGBL1 in GC cells was further used to examine the biological functions of ITGBL1.
These databases revealed that ITGBL1 was overexpressed and affected the overall survival in GC. Besides, the expression of ITGBL1 positively correlated with immune-infiltrating cells and EMT-related markers. Subsequently, molecular biology experiments verified these predictions. In GC tissues and cells, ITGBL1 was notably overexpressed. Loss-of-function studies showed that the knockdown of ITGBL1 significantly suppressed migration and invasion but promoted apoptosis in MGC803 GC cells. Furthermore, the inhibition of ITGBL1 resulted in remarkably increased protein expression levels of cadherin 1, while the expression of Vimentin, Snail, and transforming growth factor-β1 was downregulated, indicating the initiation and progression of GC caused by ITGBL1 partly via inducing EMT.
To sum up, the findings indicated that ITGBL1 acted as a valuable oncogenic factor in GC.
整合素β样 1（ITGBL1）参与多种人类恶性肿瘤。然而，关于 ITGBL1 在胃癌（GC）中的作用的信息有限。因此，本研究旨在进一步探讨 ITGBL1 在 GC 中的功能和机制。
首先，使用多个生物信息学数据库，包括 Oncomine、Tumor Immune Estimation Resource、UALCAN 和 Kaplan-Meier Plotter，预测 ITGBL1 的表达水平和预后价值，以及其与 GC 中的免疫浸润和上皮-间充质转化（EMT）的关联。定量逆转录聚合酶链反应和免疫组织化学分析用于检测 GC 组织和细胞中 ITGBL1 的表达。然后，进一步靶向沉默 GC 细胞中的 ITGBL1，以检测 ITGBL1 的生物学功能。
这些数据库表明 ITGBL1 在 GC 中过表达并影响总体生存率。此外，ITGBL1 的表达与免疫浸润细胞和 EMT 相关标志物呈正相关。随后，分子生物学实验验证了这些预测。在 GC 组织和细胞中，ITGBL1 明显过表达。功能丧失研究表明，ITGBL1 的敲低显著抑制了 MGC803 GC 细胞的迁移和侵袭，但促进了细胞凋亡。此外，抑制 ITGBL1 导致钙粘蛋白 1 的蛋白表达水平显著增加，而波形蛋白、Snail 和转化生长因子-β1 的表达下调，表明 ITGBL1 通过诱导 EMT 导致 GC 的发生和发展。
总之，研究结果表明 ITGBL1 在 GC 中是一种有价值的致癌因子。
