MiR-145-5p suppresses the proliferation, migration and invasion of gastric cancer epithelial cells via the ANGPT2/ NOD_L
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Cancer Cell International Open Access
PRIMARY RESEARCH
MiR-145-5p suppresses the proliferation, migration and invasion of gastric cancer epithelial cells via the ANGPT2/NOD_LIKE_ RECEPTOR axis Kai Zhou1†, Binbin Song2†, Ming Wei1, Jubo Fang1 and Yufen Xu2*
Abstract Objective: This study aimed to investigate the relationship among miR-145-5p, ANGPT2 and the NOD_LIKE_RECEPTOR pathway, thereby revealing the molecular mechanism of these three factors underlying the proliferation, migration and invasion of gastric cancer (GC) epithelial cells. Methods: qRT-PCR was carried out to detect the expression of miR-145-5p and ANGPT2 mRNA. Western blot was performed to test the protein levels of ANGPT2 as well as NOD1, NOD2 and NF-κB in the NOD_LIKE_RECEPTOR pathway. The targeting relationship between miR-145-5p and ANGPT2 was verified via a dual-luciferase reporter gene assay. The proliferation, migration and invasion of GC cells were detected through MTT and Transwell assays, respectively. Results: The expression of miR-145-5p was significantly down-regulated in GC cells, while that of ANGPT2 was notably up-regulated. MiR-145-5p directly bound with the 3′-UTR of ANGPT2 mRNA, thereby targeting ANGPT2 after transcription. Overexpression of miR-145-5p inhibited the proliferation, migration and invasion of GC cells by suppressing ANGPT2. Moreover, low expression of ANGPT2 affected the protein levels of NOD1, NOD2 and NF-κB in the NOD_LIKE_RECEPTOR pathway, thus weakening the abilities of cell proliferation, migration and invasion. Conclusions: MiR-145-5p plays an important role in GC epithelial cells, and it can affect cell proliferation, migration and invasion of GC cells by targeting ANGPT2 and regulating the NOD_LIKE_RECEPTOR pathway. Overall, our study further elucidates the molecular mechanism underlying the malignant progression of GC. Keywords: miR-145-5p, ANGPT2, NOD_LIKE_RECEPTOR, Gastric cancer, Proliferation, Migration and invasion Background Gastric cancer (GC) is one of the four most common malignancies worldwide with a relatively high rate of morbidity and mortality [1]. Because of unobvious
*Correspondence: [email protected] † Kai Zhou and Binbin Song contributed equally to this work 2 Department of Oncology, The First Hospital of Jiaxing, Affiliated Hospital of Jiaxing University, 1882# Zhonghuan South Road, Jiaxing 314000, China Full list of author information is available at the end of the article
symptoms in the early stage of GC, most patients are diagnosed in the advanced stage, and surgical resection is no more effective, leading to a low cure rate and poor overall prognosis [2]. In addition, the incidence of GC in young people has gradually increased [3]. Although great progress has been achieved in the diagnosis and treatment of GC in recent years, the survival rate of this disease in most countries still remains 25–30% [4]. Therefore, investigating the molecular mechanism underlying GC initiation and progression is of great importance for exploring targeted therapeutic approaches towards GC .
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