Cinobufacini inhibits epithelial-mesenchymal transition of human hepatocellular carcinoma cells through c-Met/ERK signaling pathway

Qi, Fanghua; Wang, Jinjing; Zhao, Lin; Cai, Pingping; Tang, Wei; Wang, Zhixue

doi:10.5582/bst.2018.01082

Cited by 19 publications

(10 citation statements)

References 32 publications

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“…For example, deguelin can suppress tumor angiogenesis on vascular endothelial cells by decreasing autocrine VEGF and repressing HGF-induced c-Met signaling pathways, thereby inhibiting HCC progression . Also, Cinobufacini, a well-known traditional Chinese medicine extracted from toad skins and venom glands, has a therapeutic effect in HCC (Qi et al, 2018). A study has found that Cinobufacini could suppress HepG2 cell invasion and metastasis through the inhibition of the c-Met/ERK induced EMT (Qi et al, 2018).…”

Section: Natural Compound and Herbal Medicinesmentioning

confidence: 99%

The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma

Rao

Lou

et al. 2020

Front. Cell Dev. Biol.

121

100

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Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide, leading to a large global cancer burden. Hepatocyte growth factor (HGF) and its highaffinity receptor, mesenchymal epithelial transition factor (c-Met), are closely related to the onset, progression, and metastasis of multiple tumors. The HGF/c-Met axis is involved in cell proliferation, movement, differentiation, invasion, angiogenesis, and apoptosis by activating multiple downstream signaling pathways. In this review, we focus on the function of the HGF/c-Met axis in HCC. The HGF/c-Met axis promotes the onset, proliferation, invasion, and metastasis of HCC. Moreover, it can serve as a biomarker for diagnosis and prognosis, as well as a therapeutic target for HCC. In addition, it is closely related to drug resistance during HCC treatment.

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Section: Natural Compound and Herbal Medicinesmentioning

confidence: 99%

The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma

Rao

Lou

et al. 2020

Front. Cell Dev. Biol.

121

100

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Section: Discussionmentioning

confidence: 99%

“…EMT is an important biological process induced by the c-met signaling pathway and is a crucial initiation step required for tumor migration and invasion [ 49 ]. MMPs, which are major proteolytic enzymes, have an important role in the degradation of the extracellular matrix, and thus, contribute to the regulation of tumor metastasis [ 49 ]. In the current study, silencing of FASN, FSCN1 or SPTBN1 expression in liver cancer cells led to changes in the mRNA expression of EMT-associated markers, E-cadherin, N-cadherin, vimentin and transcription factors Snail and Twist, and altered the protein expression of MMP-2 and MMP-9.…”

Section: Discussionmentioning

confidence: 99%

Identification of the fatty acid synthase interaction network via iTRAQ-based proteomics indicates the potential molecular mechanisms of liver cancer metastasis

et al. 2020

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Background Fatty acid synthase (FASN) is highly expressed in various types of cancer and has an important role in carcinogenesis and metastasis. To clarify the mechanisms of FASN in liver cancer invasion and metastasis, the FASN protein interaction network in liver cancer was identified by targeted proteomic analysis. Methods Wound healing and Transwell assays was performed to observe the effect of FASN during migration and invasion in liver cancer. Isobaric tags for relative and absolute quantitation (iTRAQ)-based mass spectrometry were used to identify proteins interacting with FASN in HepG2 cells. Differential expressed proteins were validated by co-immunoprecipitation, western blot analyses and confocal microscopy. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were performed to demonstrate the mechanism of FASN regulating metastasis. Results FASN knockdown inhibited migration and invasion of HepG2 and SMMC7721 cells. A total of, 79 proteins interacting with FASN were identified. Additionally, gene ontology term enrichment analysis indicated that the majority of biological regulation and cellular processes that the FASN-interacting proteins were associated with. Co-precipitation and co-localization of FASN with fascin actin-bundling protein 1 (FSCN1), signal-induced proliferation-associated 1 (SIPA1), spectrin β, non-erythrocytic 1 (SPTBN1) and CD59 were evaluated. Knockdown of FASN in liver cancer reduced the expression of FSCN1, SIPA1, SPTBN1 and CD59. Furthermore, inhibition of FASN, FSCN1 or SPTBN1 expression in liver cancer resulted in alterations of epithelial–mesenchymal transition (EMT)-associated markers E-cadherin, N-cadherin, vimentin and transcription factors, Snail and Twist, at the mRNA level, and changes in matrix metallopeptidase (MMP)-2 and MMP-9 protein expression. Conclusion The results suggested that the FASN-interacting protein network produced by iTRAQ-based proteomic analyses may be involved in regulating invasion and metastasis in liver cancer by influencing EMT and the function of MMPs.

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“…HGF‐induced C‐MET–dependent signal transduction promoted PKM2 nuclear translocation, and the nuclear translocation of PKM2 directly determined C‐MET–dependent cell proliferation. ERK 1/2 is an important downstream molecule for signal transduction after C‐MET activation, and it is also upstream of PKM2 in EGFR activation‐induced glioblastoma growth . Previous studies have demonstrated that EGFR‐mediated ERK1/2 activation promotes PKM2 S37 phosphorylation that determines PKM2 nuclear translocation.…”

Section: Discussionmentioning

confidence: 99%

C‐MET–dependent signal transduction mediates retinoblastoma growth by regulating PKM2 nuclear translocation

Dai

Zeng

Luo

2019

Cell Biochemistry & Function

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Mesenchymal epithelial transition (C-MET) factor overexpression has been found in many types of cancer and has served as an important molecular target for therapeutic intervention. However, the role of C-MET in retinoblastoma remains largely unclear.The present study aimed to investigate the potential role and mechanism of C-MET in Y79 retinoblastoma cells. We found that C-MET was highly expressed in Y79 retinoblastoma cells, and, in addition, the levels of C-MET were positively correlated with cell proliferation and retinoblastoma growth. Inhibition of C-MET suppressed Y79 retinoblastoma cell proliferation and tumour growth. Mechanistically, we showed that HGF-induced C-MET-dependent signal transduction resulted in ERK 1/2 phosphorylation, which subsequently promoted the nuclear translocation of PKM2. Nuclear PKM2 further interacted with histone H3 and contributed to C-MET-dependent cyclin D1 and c-Myc expression and cell proliferation. These findings highlight the role of C-MET in Y79 retinoblastoma cells and reveal a C-MET-dependent signal transduction mechanism. C-MET may be a potential therapeutic target for retinoblastoma.Significance of the study: We demonstrated a new target of retinoblastoma, C-MET. C-MET-dependent signal transduction promotes Y79 retinoblastoma cell proliferation and tumour growth through ERK 1/2/PKM2/histone H3 signalling pathway. C-MET may be a potential target for retinoblastoma therapy.

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Cinobufacini inhibits epithelial-mesenchymal transition of human hepatocellular carcinoma cells through c-Met/ERK signaling pathway

Cited by 19 publications

References 32 publications

The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma

The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma

Identification of the fatty acid synthase interaction network via iTRAQ-based proteomics indicates the potential molecular mechanisms of liver cancer metastasis

C‐MET–dependent signal transduction mediates retinoblastoma growth by regulating PKM2 nuclear translocation

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