microRNA-128-3p inhibits proliferation and accelerates apoptosis of gastric cancer cells via inhibition of TUFT1

World Journal of Surgical Oncology

Research

Xiangli Yin¹  Xiong Du²  Yanxin Li²  Bin Lian³ 

[1] Department of Pathology, Xi’an International Medical Center Hospital, No.777, Xitai Road, High-Tech Zone, 710000, Xi’an, Shaanxi, China;Department of Pathology, Yanan University Affiliated Hospital, 716000, Yan’an, Shaanxi, China;Guangzhou Huayin Medical Laboratory Center. Ltd., 510000, Guangzhou, Guangdong, China;

关键词: Gastric cancer;    MicroRNA-128-3p;    Tuftelin1;    Proliferation;    Invasion;    Epithelial-mesenchymal transition;    Apoptosis;   

DOI  :  10.1186/s12957-023-02906-0

 received in 2022-09-14, accepted in 2022-11-26,  发布年份 2022

来源: Springer

【 摘 要 】

ObjectiveGastric cancer (GC) is a malignant tumor rooting in the gastric mucosal epithelium, ranking the first among various malignant tumors. Therefore, the influence of microRNA-128-3p (miR-128-3p) by regulation of Tuftelin1 (TUFT1) on GC cells was investigated.MethodsThe expression levels of miR-128-3p and TUFT1 in GC tissues and cells were detected. The correlation between miR-128-3p expression and overall survival of GC patients was analyzed. Human GC cells MGC803 were transfected with miR-128-3p or TUFT1-related oligonucleotides to figure their roles in viability, apoptosis, invasion, as well as epithelial-mesenchymal transition (EMT). The relationship between miR-128-3p and TUFT1 was validated.ResultsmiR-128-3p expression was low and TUFT1 expression was high in GC tissues. miR-128-3p expression was positively correlated with the overall survival of patients with GC. miR-128-3p targeted TUFT1. Up-regulated miR-128-3p or suppressed TUFT1 repressed viability, invasion, and EMT, and accelerated apoptosis of GC cells. Overexpressed TUFT1 reduced miR-128-3p-mediated growth inhibition of GC cells.ConclusionThe study stresses that miR-128-3p can inhibit TUFT1 expression, thereby repressing GC cell activities.

【 授权许可】

CC BY   
© The Author(s) 2023

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