CLIC1 knockout inhibits invasion and migration of gastric cancer by upregulating AMOT-p130 expression
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RESEARCH ARTICLE
CLIC1 knockout inhibits invasion and migration of gastric cancer by upregulating AMOT‑p130 expression Y. Qiu1 · Y.‑t. Mao1 · J.‑h. Zhu1 · K. Zhao1 · J.‑f. Wang1 · J.‑m. Huang2 · G.‑q. Chang2 · Y.‑t. Guan2 · F.‑y. Huang2 · Y.‑j. Hu2 · J.‑q. Chen1 · J.‑l. Liu1 Received: 16 March 2020 / Accepted: 25 June 2020 © Federación de Sociedades Españolas de Oncología (FESEO) 2020
Abstract 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. Keywords CLIC1 · AMOT-p130 · Gastric cancer · EMT
Introduction Gastric cancer (GC) is one of the most frequently diagnosed malignant tumors in the world. There are more than 1,000,000 new cases of GC in the world each year, and the death toll is approximately 783,000 (equating to 1 for every Y. Qiu and Y.-t. Mao contributed equally to this work. * J.‑q. Chen [email protected] * J.‑l. Liu [email protected] 1
Department of Gastrointestinal Surgery, The First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, People’s Republic of China
The Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China
2
12 deaths, globally) [1]. Metastasis is still one of the leading causes of poor prognosis in patients with GC. However, there are relatively few studies on metastasis of GC, and the mechanism still needs to be elucidated. For these reasons, the exploration of key molecules involved in the metastasis of GC requires immediate attention to improve clinical outcomes. Chloride intracellular channel 1 (CLIC1), a cyclic protein of 241 amino acids, is expressed mainly in the nucleus, as well as in the cytoplasm and cell membrane of cells [2]. According to the reports in the literature, the expression of CLIC1 is increased in gallbladder carcinoma
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