Carbonic Anhydrase III Promotes Cell Migration and Epithelial–Mesenchymal Transition in Oral Squamous Cell Carcinoma

Chu, Yen-Ping; Su, Chung‐Kuang; Hsieh, Yih‐Shou; Chen, Pei‐Ni; Lin, Chiao‐Wen

doi:10.3390/cells9030704

Cited by 19 publications

(15 citation statements)

References 48 publications

(45 reference statements)

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“…EMT is a process characterized by loss of cell-cell adhesion and increase migration and invasion ability. The trans-differentiation from quiescent epithelial cells into motile mesenchymal cells is essential for tumor progression [27,28]. We observed that GDF15 expression levels were negatively correlated with adhesion molecule E-cadherin levels and positively correlated with mesenchymal marker vimentin (Fig.…”

Section: Discussionmentioning

confidence: 73%

GDF15-Mediated Cholesterol Metabolism Promotes EMT and Metastasis in Esophageal Cancer

Dong

Huang

Jiang

et al. 2020

Preprint

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Background: GDF15 is a potential biomarker for patients with esophageal cancer (EC). However, the mechanistic role of GDF15 in the invasion and metastasis of EC remains poorly understood. Methods: We determined the expression and function of GDF15 in esophageal cancer cells (ESCCs) and in patient tissue samples using western blotting, migration and invasion assays, immunohistochemistry, Co-IP assays, and quantitative real-time-PCR. In addition, a pulmonary metastatic nude mouse model was used to determine the function of GDF15. We then supplemented our experimental results with database analysis to validate our findings.Results: GDF15 was upregulated in EC, and was associated with poor differentiation, high metastasis rates and worse prognosis. GDF15 knock-down reduced the migration and invasion of ESCCs. Co-IP assays demonstrated its association with SCAP, while GDF15 knock-down decreased SCAP levels. SCAP overexpression reversed the migration, invasion and EMT in GDF15-siRNA ESCCs. However, after incubation with β-cyclodextrin (β-CD), the ability of migration and invasion was weakened, EMT was reversed again. Migration, invasion, and EMT were enhanced in GDF15-siRNA ESCCs cultured in the presence of cholesterol and were similar to GDF15-siRNA ESCCs overexpressing SCAP. In vivo, knockdown of GDF15 inhibited lung metastasis of ESCCs and was reversed by SCAP overexpression or high cholesterol diet. Increased lung metastasis after SCAP overexpression was partially suppressed by intraperitoneal injection of β-CD. In addition, we determined that GDF15 was a direct target of miR-1324, miR-1324 was down-regulated in EC tissues. MiR-1324 upregulation resulted in decreased GDF15 expression and metastasis in ESCCs. Conclusions: We demonstrated that SCAP mediated GDF15-induced the invasion and metastasis of EC by regulating cholesterol metabolism. In addition, GDF15 was shown to be a direct target of miR-1324.

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Section: Discussionmentioning

confidence: 73%

GDF15-Mediated Cholesterol Metabolism Promotes EMT and Metastasis in Esophageal Cancer

Dong

Huang

Jiang

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…EMT is a process characterized by loss of cell-cell adhesion and increase migration and invasion ability. The trans-differentiation from quiescent epithelial cells into motile mesenchymal cells is essential for tumor progression ( 28 , 29 ). We observed that GDF15 expression levels were negatively correlated with adhesion molecule E-cadherin levels and positively correlated with mesenchymal marker vimentin ( Figure 1F ).…”

Section: Discussionmentioning

confidence: 99%

SCAP Mediated GDF15-Induced Invasion and EMT of Esophageal Cancer

et al. 2020

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Background: GDF15 is a potential biomarker for patients with esophageal cancer (EC). However, the mechanistic role of GDF15 in the invasion and metastasis of EC remains poorly understood. Methods: We determined the expression and function of GDF15 in esophageal cancer cells (ESCCs) and in patient tissue samples using western blotting, migration, and invasion assays, immunohistochemistry, Co-IP assays, and quantitative real-time-PCR. In addition, a pulmonary metastatic nude mouse model was used to determine the function of GDF15. We then supplemented our experimental results with database analysis to validate our findings. Results: GDF15 was upregulated in EC, and was associated with poor differentiation, high metastasis rates, and worse prognosis. GDF15 knock-down reduced the migration and invasion of ESCCs. Co-IP assays demonstrated its association with SCAP, while GDF15 knock-down decreased SCAP levels. SCAP overexpression reversed the migration, invasion and EMT in GDF15-siRNA ESCCs. However, after incubation with β-cyclodextrin (β-CD), the ability of migration and invasion was weakened, EMT was reversed again. Migration, invasion, and EMT were enhanced in GDF15-siRNA ESCCs cultured in the presence of cholesterol and were similar to GDF15-siRNA ESCCs overexpressing SCAP. In vivo , knockdown of GDF15 inhibited lung metastasis of ESCCs and was reversed by SCAP overexpression or high cholesterol diet. Increased lung metastasis after SCAP overexpression was partially suppressed by intraperitoneal injection of β-CD. In addition, we determined that GDF15 was a direct target of miR-1324, miR-1324 was down-regulated in EC tissues. MiR-1324 upregulation resulted in decreased GDF15 expression and metastasis in ESCCs. Conclusions: We demonstrated that SCAP mediated GDF15-induced the invasion and metastasis of EC by regulating cholesterol metabolism. In addition, GDF15 was shown to be a direct target of miR-1324.

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“…The capability of c ellular migration and invasion was measured as described previously [ 28 ]. Briefly, cells seeded onto the filter inserts (8-μm pores) pre-coated with or without Matrigel for the invasion assay and migration assay, respectively.…”

Section: Methodsmentioning

confidence: 99%

Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression

Hsieh

et al. 2020

IJMS

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Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer.

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Carbonic Anhydrase III Promotes Cell Migration and Epithelial–Mesenchymal Transition in Oral Squamous Cell Carcinoma

Cited by 19 publications

References 48 publications

GDF15-Mediated Cholesterol Metabolism Promotes EMT and Metastasis in Esophageal Cancer

GDF15-Mediated Cholesterol Metabolism Promotes EMT and Metastasis in Esophageal Cancer

SCAP Mediated GDF15-Induced Invasion and EMT of Esophageal Cancer

Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression

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