ArticleExperimental and therapeutic medicine2021
The effect of splicing MST1R in gastric cancer was enhanced by lncRNA FENDRR.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The role of alternative splicing in gastric cancer.Biology direct · 2026Review
- Phosphorus Metabolism-Related Genes Serve as Novel Biomarkers for Predicting Prognosis in Bladder Cancer: A Bioinformatics Analysis.Iranian journal of public health · 2024Review
- Function of serine/arginine-rich splicing factors in hematopoiesis and hematopoietic malignancies.Cancer cell international · 2024Review
- Unveiling dysregulated lncRNAs and networks in non-syndromic cleft lip with or without cleft palate pathogenesis.Scientific reports · 2024Article
- Landscape of Druggable Molecular Pathways Downstream of Genomic CDH1/Cadherin-1 Alterations in Gastric Cancer.Journal of personalized medicine · 2022Article
- The miR-3648/FRAT1-FRAT2/c-Myc negative feedback loop modulates the metastasis and invasion of gastric cancer cells.Oncogene · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) poses a serious threat to human health worldwide. Serine/arginine rich splicing factor 1 (SRSF1) has been reported to serve regulatory roles during the tumorigenesis of GC. In addition, the macrophage stimulating 1 receptor (MST1R) signaling pathway was found to participate in the progression of GC. However, the association between MST1R and SRSF1 in the tumorigenesis of GC remains unclear. The expression levels of MST1R and the recepteur d'origine nantais (RON) Δ160 splicing variant were analyzed in cells using western blotting and immunofluorescence staining. Co-immunoprecipitation assays were used to investigate the interaction between SRSF1 and MST1R. A Cell Counting Kit-8 assay was performed to analyze cell viability. Flow cytometry and Transwell assays were used to determine cell apoptosis and invasiveness levels. The potential interaction between SFSR1 and long non-coding RNAs (lncRNAs) was investigated with an online bioinformatics tool. The findings of the present study revealed that the expression levels of MST1R and RON Δ160 were significantly upregulated in GC Kato III cells. SRSF1 was found to be regulated by the lncRNA FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR). The knockdown of SRSF1 or FENDRR downregulated the expression levels of MST1R in Kato III cells. In addition, the expression levels of RON Δ160 were markedly downregulated in Kato III cells following the knockdown of FENDRR. Meanwhile, SRSF1 directly bound to MST1R, while this phenomenon was partially reversed by FENDRR short interfering RNA. FENDRR could interact with SRSF1 in Kato III cells and the knockdown of FENDRR also induced the apoptosis of GC cells. In conclusion, the findings of the present study suggested that the lncRNA FENDRR may function as an oncogene during the progression of GC by regulating alternative splicing of MST1R and SRSF1 expression levels. lncRNA FENDRR may serve as a potential marker for the diagnosis or target for the treatment of GC.
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