CLIC1 knockout inhibits invasion and migration of gastric cancer by upregulating AMOT-p130 expression

• DOI: 10.1007/s12094-020-02445-0
• Publication Date: 2020-07-13T05:31:17Z
• Authors: Y. Qiu; Y.-t. Mao; J.-h. Zhu; K. Zhao; J.-f. Wang; J.-m. Huang; G.-q. Chang; Y.-t. Guan; F.-y. Huang; Y.-j. Hu; J.-q. Chen; J.-l. Liu
• Keywords: Immunofluorescence

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).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.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.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.