Cordycepin suppresses the migration and invasion of human liver cancer cells by downregulating the expression of CXCR4

Guo, Zhongrong; Chen, Wen; Dai, Guisen; Huang, Yadong

doi:10.3892/ijmm.2019.4391

Cited by 28 publications

(27 citation statements)

References 55 publications

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“…( 18 , 21 ) Cordycepin suppresses the migration and invasion of human liver cancer cells. ( 22 ) However, the protective effects of cordycepin against the progression of NASH and the underlying mechanisms of action of these effects remain unknown.…”

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confidence: 99%

Cordycepin Ameliorates Nonalcoholic Steatohepatitis by Activation of the AMP‐Activated Protein Kinase Signaling Pathway

Lan

Zhang

et al. 2021

Hepatology

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BaCKgRoUND aND aIMS: Nonalcoholic fatty liver disease, especially nonalcoholic steatohepatitis (NASH), has become a major cause of liver transplantation and liverassociated death. NASH is the hepatic manifestation of metabolic syndrome and is characterized by hepatic steatosis, inflammation, hepatocellular injury, and different degrees of fibrosis. However, there is no US Food and Drug Administration-approved medication to treat this devastating disease. Therapeutic activators of the AMP-activated protein kinase (AMPK) have been proposed as a potential treatment for metabolic diseases such as NASH. Cordycepin, a natural product isolated from the traditional Chinese medicine Cordyceps militaris, has recently emerged as a promising drug candidate for metabolic diseases. appRoaCH aND ReSUltS: We evaluated the effects of cordycepin on lipid storage in hepatocytes, inflammation, and fibrosis development in mice with NASH. Cordycepin attenuated lipid accumulation, inflammation, and lipotoxicity in hepatocytes subjected to metabolic stress. In addition, cordycepin treatment significantly and dose-dependently decreased the elevated levels of serum aminotransferases in mice with diet-induced NASH. Furthermore, cordycepin treatment significantly reduced hepatic triglyceride accumulation, inflammatory cell infiltration, and hepatic fibrosis in mice. In vitro and in vivo mechanistic studies revealed that a key mechanism linking the protective effects of cordycepin were AMPK phosphorylation-dependent, as indicated by the finding that treatment with the AMPK inhibitor Compound C abrogated cordycepin-induced hepatoprotection in hepatocytes and mice with NASH. CoNClUSIoN:Cordycepin exerts significant protective effects against hepatic steatosis, inflammation, liver injury, and fibrosis in mice under metabolic stress through activation of the AMPK signaling pathway. Cordycepin might be an AMPK activator that can be used for the treatment of NASH.

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confidence: 99%

Cordycepin Ameliorates Nonalcoholic Steatohepatitis by Activation of the AMP‐Activated Protein Kinase Signaling Pathway

Lan

Zhang

et al. 2021

Hepatology

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“…Results revealed a dose-dependent increase in migration, which was not linearly related to dose ( Figure 4 ). Previous authors have reported a reduction in migration of cancer cells in the presence of Cordycepin [ 15 , 16 ]. However, our study reports an increase in migration of stem cells.…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependent Effect of Cordycepin on Viability, Proliferation, Cell Cycle, and Migration in Dental Pulp Stem Cells

Boreak

Alkahtani

Alzahrani

et al. 2021

JPM

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Objective: To examine the effect of Cordycepin on the viability, proliferation, and migratory properties of dental pulp-derived mesenchymal stem cells. Materials and methods: The pulp was derived from human premolar teeth extracted for orthodontic purposes after obtaining informed consent. The samples were transferred to the laboratory for processing. DPSCs were expanded and characterized using flow cytometry and differentiation to the bone, adipose, and cartilage cells was examined. MTT Assay was performed using various concentrations of Cordycepin. The growth curve was plotted for 13 days. Cell cycle analysis was performed by flow cytometry. Migratory ability was assessed by wound healing assay. ROS generation was detected by flow cytometry. Gene expression was quantified by RT-qPCR. Statistical analysis was performed. p < 0.05 was considered as significant and p < 0.01 was considered as highly significant (* p < 0.05, and ** p < 0.01). Results: DPSCs expressed characteristic MSC-specific markers and trilineage differentiation. Cordycepin at lower concentrations did not affect the viability of DPSCs. The growth curve of cells showed a dose-dependent increase in cell numbers till the maximum dose. DPSCs treated with 2.5 µM Cordycepin was found to have a reduced G1 phase cell percentage. DPSCs treated with 2.5 µM and 5 µM Cordycepin showed a significant decrease in G2 phase cells. No significant difference was observed for S phase cells. Cordycepin treatment affected the migratory ability in DPSCs in a concentration-dependent manner. Conclusion: Cordycepin can be used at therapeutic doses to maintain stem cells.

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“…Therefore, behavioural activity after TFF2 injection with or without pre-infusion of CXCR4 is to be investigated as well [ 66 , 91 ]. Importantly, expression of CXCR4 in other tissues including digestive tract and metabolic tissues [ 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 ], could suggest a metabolic action of TFF2 via CXCR4 within these tissues.…”

Section: Tff2 Metabolic Properties and Implicationsmentioning

confidence: 99%

Trefoil Factor Family Member 2: From a High-Fat-Induced Gene to a Potential Obesity Therapy Target

Ghanemi

Yoshioka²,

St‐Amand

2021

Metabolites

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Obesity has its epidemiological patterns continuously increasing. With controlling both diet and exercise being the main approaches to manage the energy metabolism balance, a high-fat (HF) diet is of particular importance. Indeed, lipids have a low satiety potential but a high caloric density. Thus, focusing on pharmacologically targetable pathways remains an approach with promising therapeutic potential. Within this context, trefoil factor family member 2 (Tff2) has been characterized as specifically induced by HF diet rather than low-fat diet. TFF2 has also been linked to diverse neurological mechanisms and metabolic patterns suggesting its role in energy balance. The hypothesis is that TFF2 would be a HF diet-induced signal that regulates metabolism with a focus on lipids. Within this review, we put the spotlight on key findings highlighting this line of thought. Importantly, the hypothetical mechanisms pointed highlight TFF2 as an important contributor to obesity development via increasing lipids intestinal absorption and anabolism. Therefore, an outlook for future experimental activities and evaluation of the therapeutic potential of TFF2 inhibition is given. Indeed, its knockdown or downregulation would contribute to an antiobesity phenotype. We believe this work represents an addition to our understanding of the lipidic molecular implications in obesity, which will contribute to develop therapies aiming to manage the lipidic metabolic pathways including the absorption, storage and metabolism via targeting TFF2-related pathways. We briefly discuss important relevant concepts for both basic and clinical researchers.

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Cordycepin suppresses the migration and invasion of human liver cancer cells by downregulating the expression of CXCR4

Cited by 28 publications

References 55 publications

Cordycepin Ameliorates Nonalcoholic Steatohepatitis by Activation of the AMP‐Activated Protein Kinase Signaling Pathway

Cordycepin Ameliorates Nonalcoholic Steatohepatitis by Activation of the AMP‐Activated Protein Kinase Signaling Pathway

Dose-Dependent Effect of Cordycepin on Viability, Proliferation, Cell Cycle, and Migration in Dental Pulp Stem Cells

Trefoil Factor Family Member 2: From a High-Fat-Induced Gene to a Potential Obesity Therapy Target

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