scholarly journals 12-lipoxygenase promotes tumor progress by TGF-β1-mediated epithelial to mesenchymal transition and predicts poor prognosis in esophageal squamous cell carcinoma

2019 ◽  
Vol Volume 11 ◽  
pp. 8303-8313 ◽  
Author(s):  
Yan Qu ◽  
Zhihua Wen ◽  
Si Mi ◽  
Pengxiang Chen ◽  
Jianbo Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Poor Prognosis ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tumor Progress ◽  
12 Lipoxygenase ◽  
Tgf Β1

scholarly journals MELK Predicts Poor Prognosis and Promotes Metastasis in Esophageal Squamous Cell Carcinoma Via Activating the NF-κB Pathway

2021 ◽  
Author(s):  
Jiecheng Ye ◽  
Wanying Deng ◽  
Ying Zhong ◽  
Hui Liu ◽  
Baoyin Guo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Poor Prognosis ◽  
Biological Effects ◽  
Mesenchymal Transition ◽  
Iκb Kinase

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide with a low 5-year survival rate due to the lack of effective therapeutic strategies. Accumulating evidence has indicated that Maternal embryonic leucine zipper kinase (MELK) is highly expressed in several tumors and correlates with tumor development. However, the biological effects of MELK in ESCC are still unknown.Methods: We used data from ESCC patient tissue specimens and online datasets to evaluate differences in MELK expression between paired carcinoma. Two ESCC cell lines were selected and MELK was stably knocked down by small hairpin RNA (shRNA) of MELK. Cell phenotypical experiments and animal metastasis assays were performed to detect the influence of MELK knockdown in vitro and in vivo. The potential molecular mechanism of MELK-mediated ESCC metastasis was further investigated by Western blotting and Immunofluorescence staining.Results: In this study, the expression of MELK in human ESCC tissues was higher than that in adjacent normal tissues and was positively correlated with the poor prognosis of patients. Reducing MELK expression resulted in growth inhibition and suppression of the invasive ability of ESCC cells in vitro and in vivo. MELK inhibition induced alterations of epithelial-to-mesenchymal transition associated proteins. Mechanistically, MELK interacted with IκB kinase (IKK) and promoted the phosphorylation of IKK, by which MELK regulated activation of the NF-κB pathway.Conclusions: Collectively, our study reveals the function and mechanism of MELK in the cell metastasis of ESCC, which may be a potential therapeutic target for ESCC.

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