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Updated: Dec 29, 2025

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
MicroRNA‑27a‑3p promotes epithelial‑mesenchymal transition by targeting NOVA alternative splicing regulator 1 in
Kai Li1, Xiangrong Zhu2, Xihua Chen2
1Department of Gastrointestinal Surgery II, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Abstract:
NOVA alternative splicing regulator 1 (NOVA1) dysregulation has been detected in the gastric cancer microenvironment. Decreased NOVA1 expression has been linked to the progression and poor prognosis of gastric cancer; however, the role of NOVA1 in regulating epithelial‑mesenchymal transition (EMT) remains unclear in this disease. Experimental evidence has shown that miR‑27a‑3p is a potential oncogene in gastric cancer. In the present study, we observed that miR‑27a‑3p expression was increased in gastric cancer and was inversely associated with overall survival. Overexpression of miR‑27a‑3p promoted EMT in AGS gastric cancer cells. Additionally, overexpression of miR‑27a‑3p inhibited NOVA1 expression, while silencing of NOVA1 promoted EMT in AGS cells. A total of 108 gastric cancer samples were examined for NOVA1 expression by immunohistochemistry. Decreased NOVA1 expression was linked to lymph node metastasis, tumor‑node‑metastasis stage and shorter overall survival. Therefore, these results indicated that NOVA1 could be a potential tumor suppressive gene and that miR‑27a‑3p promotes EMT by targeting NOVA1 in gastric cancer.
Insights
NOVA1 acts as a tumor suppressor in gastric cancer. MicroRNA-27a-3p promotes cancer progression by inhibiting NOVA1, driving epithelial-mesenchymal transition (EMT) and leading to poor prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Dysregulation of NOVA alternative splicing regulator 1 (NOVA1) is observed in gastric cancer.
- Decreased NOVA1 expression correlates with gastric cancer progression and poor prognosis.
- The role of NOVA1 in regulating epithelial-mesenchymal transition (EMT) in gastric cancer is not well understood.
Purpose of the Study:
- To investigate the role of NOVA1 in gastric cancer.
- To explore the relationship between NOVA1, miR-27a-3p, and EMT in gastric cancer.
Main Methods:
- Analysis of miR-27a-3p expression in gastric cancer tissues and cell lines.
- Overexpression and silencing experiments in AGS gastric cancer cells to assess effects on EMT and NOVA1 expression.
- Immunohistochemical analysis of NOVA1 expression in 108 gastric cancer samples.
Main Results:
- miR-27a-3p expression was elevated in gastric cancer and associated with shorter survival.
- Overexpression of miR-27a-3p induced EMT and suppressed NOVA1 expression in AGS cells.
- NOVA1 silencing promoted EMT in AGS cells.
- Reduced NOVA1 expression in patient samples correlated with lymph node metastasis, advanced TNM stage, and poorer survival.
Conclusions:
- NOVA1 functions as a tumor suppressor gene in gastric cancer.
- miR-27a-3p promotes EMT by targeting and inhibiting NOVA1 in gastric cancer.
- NOVA1 may serve as a prognostic biomarker for gastric cancer.
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