Macrophage migration inhibitory factor promotes tumor aggressiveness of esophageal squamous cell carcinoma via activation of Akt and inactivation of GSK3β

Liu, Ruimin; Sun, Danni; Jiao, Ye-Lin; Wang, Pan; Zhang, Juan; Wang, Ming; Ma, Jing; Sun, Mingjun; Gu, Bianli; Pan, Ci; Liu, Ke; Ma, Heng; Gao, Shegan; Ma, Yuanfang; Qi, Yi-Jun

doi:10.1016/j.canlet.2017.10.018

Cited by 27 publications

(35 citation statements)

References 50 publications

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“…It has been discovered that AKT/GSK3β pathway is activated in various human malignancies (Song et al, ; Liu et al, , ). Especially, AKT/GSK3β pathway takes a main role in EMT (Xu et al, ).…”

Section: Discussionmentioning

confidence: 99%

The CNPY2 enhances epithelial‐mesenchymal transition via activating the AKT/GSK3β pathway in non‐small cell lung cancer

Lei

Guo

et al. 2018

Cell Biology International

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The survival of non-small cell lung cancer (NSCLC) is poor due to high metastasis, and the indispensable step of metastasis includes epithelial-mesenchymal transition (EMT). In the study, by analyzing the dataset of the Cancer Genome Atlas (TCGA), we found that the expression of Canopy homolog 2 (CNPY2) is increased both in adenocarcinoma and squamous cell carcinoma, which is further confirmed in NSCLC tissues. Not only that, there is a negative correlation between CNPY2 and E-cadherin expression at mRNA level. Wound healing and transwell matrix penetration assay showed that overexpression of CNPY2 promotes the capability for invasion and metastasis of NSCLC cells. Further analysis uncovered that overexpression of CNPY2 can activate the AKT/GSK3β pathway, which leads to the inactivation of GSK-3β. The inactivation of GSK-3β increases the level of Snail, and then decreases the expression of E-cadherin to promote EMT. Eventually, inhibition of AKT suppresses the malignant transformation of CNPY2-upregulated cells. The above results suggest that CNPY2 may be served as a novel therapeutic target to therapy the NSCLC.

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Section: Discussionmentioning

confidence: 99%

The CNPY2 enhances epithelial‐mesenchymal transition via activating the AKT/GSK3β pathway in non‐small cell lung cancer

Lei

Guo

et al. 2018

Cell Biology International

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“…It has been indicated that the overexpression of macrophage migration inhibitory factor (MIF) is associated with the development and progression of esophageal squamous cell carcinoma (ESCC) ( 60 , 61 ). Further study has demonstrated that the deletion of MIF attenuates Akt-dependent GSK 3β phosphorylation and restores tumor suppressor activity of GSK 3β ( 61 ). After MIF knockdown, the activation of GSK 3β prevents the transcription and expression of Snail gene, one of activators of epithelial-mesenchymal transition (EMT) ( 62 ).…”

Section: Role Of Gsk 3β In Tumorigenesismentioning

confidence: 99%

“…After MIF knockdown, the activation of GSK 3β prevents the transcription and expression of Snail gene, one of activators of epithelial-mesenchymal transition (EMT) ( 62 ). Moreover, it has also been revealed to inhibit the expression of E-cadherin in ESCC ( 61 ). GSK 3β not only inhibits cell survival and proliferation, but also restrains tumor invasion and metastasis.…”

Section: Role Of Gsk 3β In Tumorigenesismentioning

confidence: 99%

Glycogen synthase kinase 3β in tumorigenesis and oncotherapy (Review)

Lei³

et al. 2020

Oncol Rep

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Glycogen synthase kinase 3β (GSK 3β), a multifunctional serine and threonine kinase, plays a critical role in a variety of cellular activities, including signaling transduction, protein and glycogen metabolism, cell proliferation, cell differentiation, and apoptosis. Therefore, aberrant regulation of GSK 3β results in a broad range of human diseases, such as tumors, diabetes, inflammation and neurodegenerative diseases. Accumulating evidence has suggested that GSK 3β is correlated with tumorigenesis and progression. However, GSK 3β is controversial due to its bifacial roles of tumor suppression and activation. In addition, overexpression of GSK 3β is involved in tumor growth, whereas it contributes to the cell sensitivity to chemotherapy. However, the underlying regulatory mechanisms of GSK 3β in tumorigenesis remain obscure and require further in-depth investigation. In this review, we comprehensively summarize the roles of GSK 3β in tumorigenesis and oncotherapy, and focus on its potentials as an available target in oncotherapy.

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“…ESCC is characterized by a poor prognosis. The accompanying drug resistance and side effects substantially weaken the therapeutic effectiveness [11]. Recently reports have revealed that some traditional Chinese products and their extract can be used to develop effective anticancer drugs.…”

Section: Discussionmentioning

confidence: 99%

Gecko Active Components Regulates Endoplasmic Reticulum Stress to Induce the Apoptosis of KYSE150 Cells through PERK Pathway

Duan¹,

Duan²,

Huang³

et al. 2018

JBM

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Objective: Gecko active components (GACs), extracted from the powder of whole Gecko, have been reported to be effective against esophageal squamous cell carcinoma (ESCC). Endoplasmic reticulum stress (ERs) has been regarded as an important cause for pathogenesis of esophageal squamous cell carcinoma (ESCC). In this paper, we aimed to study the effect of GACS on apoptosis of human esophageal carcinoma KYSE150 cells and to analyze the underlying signaling pathway. Methods: MTT assay was used to detect the viability of KYSE150 cells, and Flow cytometry was applied to detect reactive oxygen species (ROS), calcium generation, and the level of mitochondrial membrane potential (MMP). Western blot analysis was applied to observe the expression of apoptosis-related proteins and endoplasmic reticulum stress (ERs)-related proteins in KYSE150 cells. Results: The results showed that GACs inhibited KYSE150 cell vitality in a dose-and time-dependent manner. Not only that, GACs could up-regulated ERs-related and apoptosis-related proteins expression, and the content of ROS and calcium were significantly increased, and also, the level of MMP was significantly decreased. Conclusion: The results of this report suggested that induction of apoptosis occurs through the ERs dependent signaling pathways.

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Macrophage migration inhibitory factor promotes tumor aggressiveness of esophageal squamous cell carcinoma via activation of Akt and inactivation of GSK3β

Cited by 27 publications

References 50 publications

The CNPY2 enhances epithelial‐mesenchymal transition via activating the AKT/GSK3β pathway in non‐small cell lung cancer

The CNPY2 enhances epithelial‐mesenchymal transition via activating the AKT/GSK3β pathway in non‐small cell lung cancer

Glycogen synthase kinase 3β in tumorigenesis and oncotherapy (Review)

Gecko Active Components Regulates Endoplasmic Reticulum Stress to Induce the Apoptosis of KYSE150 Cells through PERK Pathway

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