Zhi-Hao Yu1, Yue-Mei Wang2, Yu-Zhang Jiang3, Shi-Jie Ma4, Qing Zhong5, Yi-Yuan Wan5, Xiao-Wei Wang6. 1. Department of Intensive Care Unit (ICU), The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, PR China. 2. Department of Operation Anesthesiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, PR China. 3. Department of Clinical Laboratory, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, PR China. 4. Department of Gastroenterology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, PR China. 5. Department of Medical Oncology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, PR China. 6. Department of Medical Oncology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, PR China. Electronic address: wxw7352@sina.com.
Abstract
BACKGROUND: Nidogen-2 (NID2) is a ubiquitous component in the basement membrane and plays an important role in the development of malignant tumors. However, the specific function and mechanism of the NID2 gene in gastric cancer remains unclear. In this study, we aimed to investigate the role of NID2 in gastric cancer(GC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of NID2 in 67 GC tissues and adjacent normal tissues. The relationship between NID2 expression and clinicopathological features was further analyzed. In addition, we evaluated the expression of NID2 in GC based on data from the GEPIA and Kaplan-Meier Plotter database and compared the database results with our own experimental results. Invasion and wound healing assays were used to detect the function of NID2 in MKN45 and SGC7901 cells. Finally, the NID2 network and its possible related genes are constructed by the bioinformatics framework. RESULTS: The expression level of NID2 was found to be significantly over-expressed in gastric cancer cells and tissues compared with normal controls and positively associated with TNM stage, showing a poor prognosis of GC patients. In vitro experiments indicated that NID2 was able to promote the ability of invasion and migration in GC cells. Bioinformatics prediction showed NID2 might regulate the progression of GC via protein digestion and absorption, amoebiasis, PI3K-AKt-signaling pathway, focal adhesion and ECM-receptor interaction pathways. CONCLUSION: Our study demonstrates that up-regulated NID2 plays an important role in promoting the invasion and migration of GC cells and has a potential of being a novel biomarker for diagnosis, treatment and prognosis of GC in the future.
BACKGROUND:Nidogen-2 (NID2) is a ubiquitous component in the basement membrane and plays an important role in the development of malignant tumors. However, the specific function and mechanism of the NID2 gene in gastric cancer remains unclear. In this study, we aimed to investigate the role of NID2 in gastric cancer(GC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of NID2 in 67 GC tissues and adjacent normal tissues. The relationship between NID2 expression and clinicopathological features was further analyzed. In addition, we evaluated the expression of NID2 in GC based on data from the GEPIA and Kaplan-Meier Plotter database and compared the database results with our own experimental results. Invasion and wound healing assays were used to detect the function of NID2 in MKN45 and SGC7901 cells. Finally, the NID2 network and its possible related genes are constructed by the bioinformatics framework. RESULTS: The expression level of NID2 was found to be significantly over-expressed in gastric cancer cells and tissues compared with normal controls and positively associated with TNM stage, showing a poor prognosis of GC patients. In vitro experiments indicated that NID2 was able to promote the ability of invasion and migration in GC cells. Bioinformatics prediction showed NID2 might regulate the progression of GC via protein digestion and absorption, amoebiasis, PI3K-AKt-signaling pathway, focal adhesion and ECM-receptor interaction pathways. CONCLUSION: Our study demonstrates that up-regulated NID2 plays an important role in promoting the invasion and migration of GC cells and has a potential of being a novel biomarker for diagnosis, treatment and prognosis of GC in the future.
Authors: Maria Urbanova; Verona Buocikova; Lenka Trnkova; Sabina Strapcova; Viera Horvathova Kajabova; Emma Barreto Melian; Maria Novisedlakova; Miroslav Tomas; Peter Dubovan; Julie Earl; Jozef Bizik; Eliska Svastova; Sona Ciernikova; Bozena Smolkova Journal: Int J Mol Sci Date: 2022-02-14 Impact factor: 5.923