Abstract
BackgroundThe previous investigations have identified that long non-coding RNA (lncRNAs) act as crucial regulators in gastric carcinoma. However, the function of lncRNA MIR4435-2HG in the modulation of gastric carcinoma remains elusive. Here, we aimed to explore the role of MIR4435-2HG in gastric carcinoma.MethodThe Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were applied to select the differently expressed lncRNAs in gastric carcinoma. The qRT-PCR was applied to analyze MIR4435-2HG expression in carcinoma tissues and cell lines. The effect of MIR4435-2HG on proliferation, invasion, migration, and apoptosis of gastric carcinoma cells was detected by Cell Counting Kit-8 (CCK-8) assays, transwell assays, and flow cytometry in vitro. A subcutaneous tumor model was constructed to examine the tumor growth of gastric carcinoma cells after knocking out MIR4435-2HG. RNA immunoprecipitation and luciferase reporting assays were applied to evaluate the interaction of MIR4435-2HG, miR-138-5p, and Sox4.ResultsThe bioinformatics analysis based on TCGA and GEO databases indicated that MIR4435-2HG was obviously elevated in gastric carcinoma samples. The qRT-PCR analysis revealed that MIR4435-2HG was upregulated in clinical gastric carcinoma tissues and cells. The high expression of MIR4435-2HG is associated with the poor survival rate of patients. The knockout of MIR4435-2HG could repress the proliferation, invasion, migration, and epithelial–mesenchymal transition (EMT) and accelerate the apoptosis of gastric carcinoma cells. Moreover, the deletion of MIR4435-2HG was able to attenuate the tumor growth in vivo. Mechanically, we identified that MIR4435-2HG enhanced Sox4 expression by directly interacting with miR-138-5p as a competitive endogenous RNA (ceRNA) in gastric carcinoma cells, in which Sox4 was targeted by miR-138-5p.ConclusionMIR4435-2HG is elevated in gastric carcinoma cells and contributes to the growth, metastasis, and EMT of gastric carcinoma cells by targeting miR-138-5p/Sox4 axis. MIR4435-2HG may be applied as a potential therapeutic target in gastric carcinoma.
Highlights
Gastric carcinoma is a common malignancy of the digestive tract system
The differently expressed Long non-coding RNAs (lncRNAs) in gastric carcinoma were analyzed in Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA), and we identified that MIR4435-2HG was elevated in gastric carcinoma, indicating that MIR4435-2HG might play a crucial function in gastric carcinoma cells
The expression of MIR4435-2HG in clinical gastric carcinoma tissues and cell lines was tested using qRT-PCR, and we found that MIR4435-2HG expression was enhanced in gastric carcinoma (Figures 1C, E)
Summary
Gastric carcinoma is a common malignancy of the digestive tract system. It has been indicated that the progression of gastric carcinoma is triggered by the interaction of various environmental carcinogenic factors [1, 2]. Epithelial–mesenchymal transition (EMT) is closely correlated with the metastasis in gastric carcinoma cells [6, 7]. The previous studies have demonstrated that the progression of EMT was induced in invasion and metastasis of gastric carcinoma cells [8], but the mechanism of EMT is still under exploration. The previous investigations have identified that long non-coding RNA (lncRNAs) act as crucial regulators in gastric carcinoma. The function of lncRNA MIR4435-2HG in the modulation of gastric carcinoma remains elusive. We aimed to explore the role of MIR4435-2HG in gastric carcinoma
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
