Journal
CLINICAL & TRANSLATIONAL ONCOLOGY
Volume 23, Issue 3, Pages 514-525Publisher
SPRINGER INT PUBL AG
DOI: 10.1007/s12094-020-02445-0
Keywords
CLIC1; AMOT-p130; Gastric cancer; EMT
Categories
Funding
- Guangxi Medical and Health Fund [Z2015526]
- Science Foundation for Young Scientists of Guangxi Medical University [GXMUYSF201502]
- Natural Science Foundation of Guangxi [2016GXNSFAA380180]
- Guangxi Medical University College Students Innovation and Entrepreneurship Training Program Project 2019 [201910598091]
- National Natural Science Foundation of China [81360370]
- Guangxi Scientific Research and Technology Development Project [AB18126058]
- Education Department Foundation for Innovation Team of Guangxi Zhuang Autonomous Region
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The study found that high CLIC1 expression was significantly associated with low AMOT-p130 expression in GC tissues. Silencing CLIC1 expression reduced the invasive and migratory abilities of tumor cells, which were induced by the upregulation of AMOT-p130. AMOT-p130 inhibits the invasive and migratory abilities of GC cells by inhibiting epithelial-mesenchymal transition.
Purpose To explore the regulatory relationship between Chloride intracellular channel 1 (CLIC1) and Angiomotin (AMOT)-p130, and reveal the role of AMOT-p130 in gastric cancer (GC). Methods Immunohistochemistry was performed to analyze the expression of CLIC1 and AMOT-p130 in GC tissues and adjacent tissues. The expression of AMOT-p130 upon CLIC1 silencing was analyzed using RT-PCR, western blot, and immunofluorescence in GC cells. Transwell and wound-healing assays were performed to detect migration and invasion in GC cells. The changes in EMT-related proteins were detected using western blot. Results Our study found that high CLIC1 expression was significantly associated with low AMOT-p130 expression in GC tissues. Silencing CLIC1 expression in MGC-803 cells (MGC-803 CLIC1 KO) and AGS cells (AGS CLIC1 KO) decreased the invasive and migratory abilities of tumor cells, which were induced by the upregulation of AMOT-p130. Subsequently, we demonstrated that AMOT-p130 inhibits the invasive and migratory abilities of GC cells by inhibiting epithelial-mesenchymal transition. Conclusions Our study suggests that AMOT-p130 could inhibit epithelial-mesenchymal transition in GC cells. CLIC1 may participate in the metastatic progression of GC by downregulating the expression of AMOT-p130.
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