CLIC1 knockout inhibits invasion and migration of gastric cancer by upregulating AMOT-p130 expression
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Y. Qiu [1] ; Y.-t. Mao [1] ; J.-h. Zhu [1] ; K. Zhao [1] ; J.-f. Wang [1] ; J.-m. Huang [1] ; G.-q. Chang [1] ; Y.-t. Guan [1] ; F.-y. Huang [1] ; Y.-j. Hu [1] ; J.-q. Chen [1] ; J.-l. Liu [1]
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[1] Guangxi Medical University
Guangxi Medical University
China
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- Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 23, Nº. 3 (March), 2021, págs. 514-525
- Idioma: inglés
- Texto completo no disponible (Saber más ...)
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Resumen
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.
