Nerigoside suppresses colorectal cancer cell growth and metastatic potential through inhibition of ERK/GSK3β/β-catenin signaling pathway

Wen, Shiyuan; Chen, Yanyan; Deng, Chun-Miao; Zhang, Cui-qiong; Jiang, Miaomiao

doi:10.1016/j.phymed.2018.12.033

Cited by 30 publications

(20 citation statements)

References 29 publications

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“…Phosphorylated Akt (p-Akt) can phosphorylate GSK3β and inhibit its kinase activity, leading to the inactivation of GSK3β [ 39 ]. Decreased GSK3β alleviates restraint on β-catenin [ 40 ], contributing to the accumulated β-catenin entry into the nucleus to activate gene transcription and interacts with TCF/LEF and ultimately triggers the transcription of target genes including snail [ 41 , 42 ]. As a direct downstream gene of snail, the expression of epithelial biomarker E-cadherin was significantly downregulated (Fig.…”

Section: Discussionmentioning

confidence: 99%

ARHGAP10 inhibits the epithelial–mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway

et al. 2021

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Background Rho GTPase activating protein 10 (ARHGAP10) has been implicated as an essential element in multiple cellular process, including cell migration, adhesion and actin cytoskeleton dynamic reorganization. However, the correlation of ARHGAP10 expression with epithelial–mesenchymal transition (EMT) in lung cancer cells is unclear and remains to be elucidated. Herein, we investigated the relationship between the trait of ARHGAP10 and non-small cell lung cancer (NSCLC) pathological process. Methods Immunohistochemistry was conducted to evaluate the expression of ARHGAP10 in NSCLC tissues. CCK-8 assays, Transwell assays, scratch assays were applied to assess cell proliferation, invasion and migration. The expression levels of EMT biomarkers and active molecules involved in PI3K/Akt/GSK3β signaling pathway were examined through immunofluorescence and Western blot. Results ARHGAP10 was detected to be lower expression in NSCLC tissues compared with normal tissues from individuals. Moreover, overexpression of ARHGAP10 inhibited migratory and invasive potentials of A549 and NCI-H1299 cells. In addition, ARHGAP10 directly mediated the process of EMT via PI3K/Akt/GSK3β pathway. Meanwhile, activation of the signaling pathway of insulin-like growth factors-1 (IGF-1) reversed ARHGAP10 overexpression regulated EMT in NSCLC cells. Conclusion ARHGAP10 inhibits the epithelial–mesenchymal transition in NSCLC via PI3K/Akt/GSK3β signaling pathway, suggesting agonist of ARHGAP10 may be an optional remedy for NSCLC patients than traditional opioids.

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Section: Discussionmentioning

confidence: 99%

ARHGAP10 inhibits the epithelial–mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway

et al. 2021

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“…Based on this report, we speculated that Akt-induced β-catenin Ser552 phosphorylation may be involved in cisplatin-induced PD-L1 expression in HCC cells. For MEK/ERK signaling pathway, multiple evidence showed that ERK can phosphorylate GSK-3β at Ser9 residue, resulting in the decreased β-catenin degradation in cancer cells (Caraci et al, 2008;Wen et al, 2019). Accumulated β-catenin in the cytoplasm then translocated into the nucleus where it interacts with T-cell factor/lymphoid enhancer factor family transcription factors to regulate target gene expression (Kypta & Waxman, 2012;Pez et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

HGF/c‐MET pathway contributes to cisplatin‐mediated PD‐L1 expression in hepatocellular carcinoma

Zhang

Yang

Yao

et al. 2021

Cell Biology International

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Cisplatin has been reported to promote the expression of programmed cell death ligand-1 (PD-L1) in some cancer cells. However, the underlying mechanism through which PD-L1 is transcriptionally regulated by cisplatin in hepatocellular carcinoma (HCC) cells remains largely unknown. In the present study, we found that the expression of hepatocyte growth factor (HGF), p-Akt, p-ERK, and PD-L1 was increased in cisplatin-treated SNU-368 and SNU-739 cells. HGF stimulation also increased PD-L1 expression in these cells. Moreover, Inhibition of HGF/c-MET, PI3K/Akt, and MEK/ERK signaling pathways can dramatically block cisplatin or HGF-induced PD-L1 expression in SNU-368 and SNU-739 cells. In vivo, combination PHA665752 with cisplatin significantly reduced tumor weight with increased infiltration of CD8 + T cells in the tumor. Taken together, our study suggested that HGF/c-Met axis-induced the activation of PI3K/Akt and MEK/ERK pathways contributes to cisplatin-mediated PD-L1 expression. These findings may provide an alternative avenue for the treatment of HCC.

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“…Glycogen Synthase Kinase 3β (GSK-3β) is a constitutive multifunctional serine /threonine kinase that induces tumor cell apoptosis through the destruction of oncogene products by the proteasome destruction [5]. It was reported that Nerigoside induced apoptosis in colorectal cancer cells (HT29, SW620) by inhibiting the ERK/GSK-3β/β-catenin signaling pathway [6]. Moreover, GSK-3β is closely related to the function of the mitochondrial apoptotic pathway.…”

Section: Introductionmentioning

confidence: 99%

The effect of GSK-3β in arsenic-induced apoptosis of malignant tumor cells: a systematic review and meta-analysis

Gào

Deng

Ran

et al. 2022

Toxicology Mechanisms and Methods

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Arsenic has been reported to induce apoptosis in malignant tumor cells, therefore, it may be regarded as a treatment for some cancers. The mitochondrial apoptosis pathway, mediated by GSK-3β, plays an important role in tumor cell apoptosis. Nonetheless, the regulation of GSK-3β by arsenic remains controversial.Materials and Methods ： We included 19 articles, which conducts the role of GSK-3β in the process of arsenic-induced tumor cell apoptosis by the meta-analysis.Results: Compared with the control group, the expression of GSK-3β (SMD= -0.92,95% CI (-1.78,-0.06)), p-Akt (SMD= -5.46,95% CI (-8.67,-2.24)) were reduced in the arsenic intervention group. Meanwhile, the combined treatment of arsenic and Akt agonist can inhibit the expression of p-GSK-3β. Using the dose and time subgroup analysis, it was shown that the low-dose and sub-chronic arsenic exposure could inhibit the expression of p-Akt (P<0.05). In the subgroup analysis of GSK-3β sites, arsenic could inhibit p-Akt and GSK-3β (Ser9) (SMD = -0.95, 95% CI (-1.56, -0.33)). There was a dose-related effect seen between arsenic (≤8 μmol/L) and p-GSK-3β, and the expression of p-GSK-3β was gradually followed by the arsenic dose. When arsenic acted on GSK-3β (ser9), the expression of Mcl-1 and pro-caspase-3 were dropped, while the loss rate of mitochondrial membrane potential and cleaved-caspase-3 were increased significantly (P<0.05). Conclusion:This study revealed that arsenic could inhibit the expression of GSK-3β (Ser9) and then induce tumor cell apoptosis. It might be correlated with arsenic inhibiting p-Akt, down-regulating GSK-3β, and triggering the Mcl-1-mediated mitochondrial apoptosis pathway.

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Nerigoside suppresses colorectal cancer cell growth and metastatic potential through inhibition of ERK/GSK3β/β-catenin signaling pathway

Cited by 30 publications

References 29 publications

ARHGAP10 inhibits the epithelial–mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway

ARHGAP10 inhibits the epithelial–mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway

HGF/c‐MET pathway contributes to cisplatin‐mediated PD‐L1 expression in hepatocellular carcinoma

The effect of GSK-3β in arsenic-induced apoptosis of malignant tumor cells: a systematic review and meta-analysis

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