Abstract
The aim of the present study was to investigate whether the JWA gene regulates the proliferation, migration and invasion of human esophageal squamous cell carcinoma (ESCC) and normal human esophageal cell lines through mitogen-activated protein kinase (MAPK) signal transduction pathways. The role of JWA in proliferation, migration, invasion and apoptosis was investigated in the Eca109 human ESCC and HET-1A normal human esophageal cell lines via transfection with JWA-small interfering (si)RNA. Western blot analysis was conducted to observe the effect of JWA on apoptosis and the regulatory effect of JWA on proliferation was determined using a thiazolyl blue tetrazolium bromide (MTT) assay. Cellular migration and invasion were analyzed via a Transwell assay. In addition, the expression levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 MAPK following JWA-siRNA transfection were detected by western blot analysis and compared with those of untreated cells. The downregulation of JWA protein decreased apoptosis and increased the proliferation, migration and invasion of the Eca109 and HET-1A cell lines. In the Eca109 cell line, the expression levels of phosphorylated (p)-ERK1/2 and p-JNK, but not those of p-p38, decreased significantly in the JWA siRNA group compared with those in the control groups. However, in the HET-1A cell line, JWA-siRNA transfection significantly inhibited the expression of p-p38 and demonstrated no effect on the expression levels of p-ERK1/2 and p-JNK. In conclusion, the JWA gene may regulate the ESCC and human esophageal cell lines through MAPK signaling pathways via different regulatory mechanisms.
Highlights
The mitogen-activated protein kinase (MAPK) pathways are important signal transduction pathways that are key in many metabolic processes [1,2]
The extracellular signal-regulated kinase (ERK) pathway participates in regulating cell differentiation, invasion, metastasis and opposing apoptosis. p38 MAPK has been identified to regulate microtubule polymerization and depolymerization [4]
RNA interference was used to interfere with the JWA gene in the Eca109 and HET-1A cells
Summary
The mitogen-activated protein kinase (MAPK) pathways are important signal transduction pathways that are key in many metabolic processes [1,2]. Three predominant MAPK family members have been identified; extracellular signal-regulated kinase (ERK), c‐Jun N‐terminal kinase (JNK; known as stress-activated protein kinase) and the p38 group of protein kinases [3]. The ERK pathway participates in regulating cell differentiation, invasion, metastasis and opposing apoptosis. The expression levels of JWA have been observed to be lower in malignant tumor tissues compared with those in non‐tumor tissues [5,6,7,8,9]. Previous studies in mice and cervical carcinoma HeLa cells in vitro have shown that the expression level of JWA affects tumor proliferation, invasion and apoptosis via the MAPK pathway [9,10]. To the best of our knowledge, the association between JWA and MAPK pathways in human esophageal cell lines has not been identified
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