학술논문

Long noncoding RNA MIR99AHG promotes gastric cancer progression by inducing EMT and inhibiting apoptosis via miR577/FOXP1 axis
Document Type
Academic Journal
Source
Cancer Cell International. August 27, 2020, Vol. 20 Issue 1
Subject
Analysis
Development and progression
Health aspects
Stomach cancer -- Development and progression
Apoptosis -- Analysis -- Health aspects
Cancer -- Development and progression
Genes -- Analysis -- Health aspects
Antisense RNA -- Analysis -- Health aspects
Language
English
Abstract
Author(s): Qingyang Meng[sup.1], Xiangjun Wang[sup.2], Tongqing Xue[sup.3], Qiangfang Zhao[sup.3], Wei Wang[sup.3] and Kun Zhao[sup.3] Background Gastric cancer (GC) is the leading cause of cancer-related mortality worldwide [1]. The genesis and [...]
Background Long non-coding RNAs (lncRNAs) play a vital role in the genesis and development of human cancer. LncRNA MIR99AHG has been reported to be upregulated in acute myeloid leukemia (AML); however, its function in gastric cancer (GC) is still not clear. Here we were aiming to screen the prognostic lncRNA candidates and to explore the function of MIR99AHG in GC. Methods We have preliminarily screened some candidate lncRNA biomarkers in GC tissues through analyzing microarray datasets. The expression level of MIR99AHG in GC cell lines and tissues was monitored via qPCR. Survival analysis was performed with the patients of our hospital and TCGA database cases. CCK-8 assay, trans-well assay and flow cytometry were performed to determine cell proliferation, invasion, migration and apoptosis. Meanwhile, a target of MIR99AHG was predicted and identified by luciferase reporter gene detection experiments. Results MIR99AHG was strongly up-regulated in human GC and contributed to cancer progression. Kaplan-Meier analysis revealed that up-regulating MIR99AHG expression was positively correlated with unfavorable overall survival (P < 0.01) of patients from our hospital and TCGA database. Knockdown of MIR99AHG expression inhibited cell proliferation, invasion, migration and promoted cell apoptosis. Moreover, MIR99AHG worked as an oncogenic gene though competing for endogenous RNA (ceRNA) of miR-577. Conclusions Our findings suggested that MIR99AHG contributes to malignant phenotypes of GC and may become a promising therapeutic target. Keywords: Gastric cancer, MIR99AHG, miR-577, lncRNA, ceRNA, miRNA, FOXP1