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

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...

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Veröffentlicht in:Clinical & translational oncology 2021-03, Vol.23 (3), p.514-525
Hauptverfasser: Qiu, Y., Mao, Y.-t., Zhu, J.-h., Zhao, K., Wang, J.-f., Huang, J.-m., Chang, G.-q., Guan, Y.-t., Huang, F.-y., Hu, Y.-j., Chen, J.-q., Liu, J.-l.
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Sprache:eng
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Zusammenfassung: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.
ISSN:1699-048X
1699-3055
DOI:10.1007/s12094-020-02445-0