Soluble epoxide hydrolase inhibition ameliorates proteinuria-induced epithelial-mesenchymal transition by regulating the PI3K-Akt-GSK-3β signaling pathway

2015 ◽  
Vol 463 (1-2) ◽  
pp. 70-75 ◽  
Author(s):  
Yaoxian Liang ◽  
Ziyang Jing ◽  
Hui Deng ◽  
Zhengqian Li ◽  
Zhen Zhuang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Epoxide Hydrolase ◽  
Epithelial Mesenchymal Transition ◽  
Soluble Epoxide Hydrolase ◽  
Mesenchymal Transition ◽  
Gsk 3Β

scholarly journals CHN1 promotes epithelial–mesenchymal transition via the Akt/GSK-3β/Snail pathway in cervical carcinoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Haoqi Zhao ◽  
Lan Wang ◽  
Shufang Wang ◽  
Xihua Chen ◽  
Min Liang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lymph Node ◽  
Signaling Pathway ◽  
Cervical Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Xenograft Tumor ◽  
Mesenchymal Transition ◽  
Gsk 3Β ◽  
Related Proteins

Abstract Background Metastasis and invasion are crucial in determining the mortality of cervical carcinoma (CC) patients. The epithelial–mesenchymal transition (EMT) is now a universal explanation for the mechanisms of tumor metastasis. Α-chimeric protein (α-chimaerin, CHN1) plays an important role in the regulation of signal transduction and development. However, the molecular regulatory relationships between CHN1 and CC progression in relation to EMT have not yet been identified. Methods The expression of CHN1 in CC tissues, adjacent tissues, and lymph node metastases from CC patients was detected by immunohistochemistry. Upregulation and knockdown of CHN1 were achieved by transfection of CC cells. The effect of CHN1 on cell proliferation was determined by CCK-8 and plate clone formation assays. Changes in migration and invasion capabilities were evaluated using scratch migration and transwell invasion assays. The effect of CHN1 overexpression and interference on xenograft tumor growth was determined by tumor weight and pathological analyses. The expression of EMT-related mRNAs was measured by qRT-PCR in transfected CC cells. EMT-related proteins and Akt/GSK-3β/Snail signaling pathway-related proteins were also evaluated by western blotting. Results CHN1 was overexpressed in CC tissues and was associated with lymph node metastasis and low survival in CC patients. Overexpression of CHN1 promoted cell proliferation, migration, and invasion in CC cells. In contrast, silencing of CHN1 inhibited these phenomena. Overexpression of CHN1 promoted tumor formation in an in vivo xenograft tumor mouse model, with increased tumor volumes and weights. In addition, CHN1 induced the expression of EMT-related transcription factors, accompanied by the decreased expression of epithelial markers and increased expression of mesenchymal markers. The Akt/GSK-3β/Snail signaling pathway was activated by overexpression of CHN1 in vitro, and activation of this pathway was inhibited by the signaling pathway inhibitor LY294002. Conclusion These results suggest that CHN1 promotes the development and progression of cervical carcinoma via the Akt/GSK-3β/Snail pathway by inducing EMT.

scholarly journals 14-3-3ζ and aPKC-ι synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway

Oncotarget ◽  
2016 ◽  
Vol 7 (34) ◽  
pp. 55191-55210 ◽  
Author(s):  
Yan Yang ◽  
Yan Liu ◽  
Jun-chuang He ◽  
Jian-ming Wang ◽  
Peter Schemmer ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Gsk 3Β

scholarly journals CHN1 Promotes EMT via the Akt / GSK-3β / Snail Pathway in Cervical Carcinoma

2021 ◽  
Author(s):  
Haoqi Zhao ◽  
Lan Wang ◽  
Shufang Wang ◽  
Xihua Chen ◽  
Min Liang ◽  
...  
Keyword(s):  
Lymph Node ◽  
Signaling Pathway ◽  
Cervical Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Xenograft Tumor ◽  
Regulatory Relationship ◽  
Mesenchymal Transition ◽  
Gsk 3Β ◽  
Related Proteins

Abstract Background: Metastasis and invasion are key points to lead the mortality of cervical squamous cell carcinoma (CSCC). Epithelial–mesenchymal transition (EMT) is now a universal explanation for the mechanisms of tumor metastasis. Α-chimeric protein (α-chimaerin, CHN1) plays an important role in the regulation of signal transduction and development. However, the molecular regulatory relationship between CHN1 and CSCC progression involved EMT has not been identified.Methods: The expression of CHN1 in CSCC tissues, adjacent tissues, and lymph node metastases of CSCC patients was detected by immunohistochemistry assay. Upregulation and knockdown of CHN1 was achieved by transfecting the plasmid into CSCC cells. The effect of CHN1 on proliferation was determined by CCK-8 and plate clone formation assay. Changes in migration and invasion capabilities were evaluated by scratch migration assay and trans-well invasion assay. The effect of CHN1 overexpression and interference on xenograft tumor growth was determined by measuring tumor weight and pathological analysis. The expression of EMT-related mRNA was measured by qRT-PCR assay in transfected CSCC cells. EMT-related proteins and Akt / GSK-3β / Snail signaling pathway-related proteins were also evaluated by using western blotting assay.Results: CHN1 was overexpression in CSCC tissues and was associated with lymph node metastasis and low survival of CSCC patients. The overexpression CHN1 promoted cell proliferation, migration and invasion bility in CSCC cells. On the contrary, silencing CHN1 inhibited these phenomena. In vivo experiments, the overexpression of CHN1 promoted tumors formed in xenograft tumor mouse model, with increased volume and weight of xenograft tumor. In addition, CHN1 induced the expression of EMT related transcription factors, accompanied by the decreased expression of epithelial markers and the increased expression of mesenchymal markers. The Akt / GSK-3β / Snail signaling pathway was activated by the overexpression of CHN1 in vitro, and the activation of the pathway was inhibited by signaling pathway inhibitor LY294002.Conclusion: These results suggest that CHN1 promoted development and progression in cervical carcinoma via of the Akt / GSK-3β / Snail pathway by inducing EMT.

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