Curcumol inhibits EBV-positive Nasopharyngeal carcinoma migration and invasion by targeting nucleolin

Guan, Xingying; Yu, Dan; Huangfu, Mengjie; Huang, Zhiyi; Dou, Tong; Liu, Yisa; Zhou, Leyuan; Li, Xumei; Wang, Lin; Li, Haiping; Wang, Juan; Xu, Chen

doi:10.1016/j.bcp.2021.114742

Cited by 16 publications

(7 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We examined the changes in TNF, VEGFA, and IL6 proteins after Celastrol treatment. Several studies have found that VEGFA is highly expressed in NPC cells and is associated with cell proliferation, invasion and metastasis, chemosensitivity, radiosensitivity, and other phenotypes of cancer cells ( Chen et al, 2019 ; Chen et al, 2020 ; Guan et al, 2021 ). High expression of TNF is associated with macrophage polarization and may be an independent prognostic factor for NPC ( Yu et al, 2019 ; Mardhiyah et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Exploration of the effect of Celastrol on protein targets in nasopharyngeal carcinoma: Network pharmacology, molecular docking and experimental evaluations

et al. 2022

View full text Add to dashboard Cite

Background: Celastrol, an important extract of Tripterygium wilfordii, shows strong antitumor activity in a variety of tumors including nasopharyngeal carcinoma (NPC). However, little is known about its targets in NPC. We aimed to screen the key gene targets of Celastrol in the treatment of NPC by means of in silico analyses (including network pharmacology and molecular docking) and experimental evaluations.Methods: The main target genes of Celastrol and the genes related to NPC were obtained by retrieving the relevant biological databases, and the common targets were screened. Protein-protein interaction analysis was used to screen the hub genes. Then, a “compound-target-disease” network model was created and molecular docking was used to predict the binding of Celastrol to the candidate hub proteins. Afterward, the expression changes of the candidate genes under the administration of Celastrol were verified in vitro and in vivo.Results: Sixty genes common to Celastrol and NPC were screened out, which may be related to numerous biological processes such as cell proliferation, apoptosis, and tube development, and enriched in various pathways such as PI3K- Akt, EGFR tyrosine kinase inhibitor resistance, and Apoptosis. The tight binding ability of the candidate hub proteins (TNF, VEGFA, and IL6) to Celastrol was predicted by molecular docking [Docking energy: TNF, −6.08; VEGFA,−6.76; IL6,−6.91(kcal/mol)]. In vitro experiments showed that the expression of TNF and VEGFA decreased while the expression of IL6 increased in NPC cells (CNE2 and HONE1) treated with Celastrol. In vivo experiments suggested that Celastrol significantly reduced the weight and volume of the transplanted tumors in tumor-bearing mice in vivo. The expression of TNF, VEGFA, and IL6 in the transplanted tumor cells could be regulated by using Celastrol, and the expression trends were consistent with the in vitro model.Conclusion: Several gene targets have been filtered out as the core targets of Celastrol in the treatment of NPC, which might be involved in a variety of signaling pathways. Hence, Celastrol may exert its anti-NPC activity through multiple targets and multiple pathways, which will provide new clues for further research. Future experiments are warranted to validate the findings.

show abstract

Section: Discussionmentioning

confidence: 99%

Exploration of the effect of Celastrol on protein targets in nasopharyngeal carcinoma: Network pharmacology, molecular docking and experimental evaluations

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Our team member Juan Wang found that NCL is a protein target of curcumol in nasopharyngeal carcinoma cells [16]. It is high expressed most cancer cells and closely related with tumor tumorigenesis, migration and invasion [31,32]. So, NCL is a potential target for anticancer [33,34].…”

Section: Discussionmentioning

confidence: 99%

Curcumol Inhibit Breast Cancer Growth Via NCL/ERα36 And PI3K/AKT Pathway

Wei

Wang

Dou

et al. 2021

Preprint

View full text Add to dashboard Cite

Purpose: This study is to investigate the effect and mechanism of curcumol on ERα36 positive breast cancer cells, and the relationship between curcumol’s target protein nucleolin (NCL) and ERα36. Methods: The anti-tumor effect of curcumol were quantified via MTT assay, colony formation and cycle arrest respectively. The expression of ERα36, NCL and the proteins involved in PI3K/AKT signaling were evaluated by western blotting. The interaction between two proteins were detected using co-immunoprecipitation (Co-IP) and immunofluorescence assay. Mouse xenograft model was established to verify the role of ERα36 in breast cancer cells and curcumol’s effect on ERα36 positive cancer cells. Results: Curcumol inhibited the cell growth, caused cell cycle arrest, decreased cell cycle related-proteins and inactivated PI3K/AKT pathway in ERα36 positive breast cancer cells. There is a positive correlation between NCL and ERα36 in breast cancer cells. In addition, ERα36 bound to NCL, the two proteins were distributed in the nucleus, cytoplasm and on the plasma membrane, where their expression were obviously decreased by curcumol. Moreover, NCL silenced by NCL siRNA blocked the cell cycle progress and inhibited the activation of PI3K/AKT in MDA-MB-231 cells, while overexpressed ERα36 increased the expression of NCL, promoted cell cycle progress and enhanced the activity of PI3K/AKT in MCF-7 cells. NCL knockdown or ERα36 overexpressed all attenuated the effect of curcumol on breast cancer cells. Conclusion: Curcumol reduced the proliferation of breast cancer cells by targeting NCL/ERα36 and inactivated PI3K/AKT pathway.

show abstract

“…Curcumol is an essential oil of Rhizoma Curcumae (Lou et al 2010) and recent studies have shed some light on its capacity in tumor suppression (Sheng et al 2021). Curcumol suppresses ability of nasopharyngeal carcinoma cells in migration and invasion via inhibiting PI3K/Akt axis and reducing expression of NCL (Guan et al 2021). Curcumol has capacity of inducing both apoptosis and autophagy in nasopharyngeal cancer cells to reduce proliferation (Wang et al 2021e).…”

Section: The Pharmacological Intervention In Doxorubicin Chemosensiti...mentioning

confidence: 99%

miRNAs as short non-coding RNAs in regulating doxorubicin resistance

Mirzaei,

Paskeh,

Moghadam

et al. 2023

J. Cell Commun. Signal.

View full text Add to dashboard Cite

Curcumol inhibits EBV-positive Nasopharyngeal carcinoma migration and invasion by targeting nucleolin

Cited by 16 publications

References 23 publications

Exploration of the effect of Celastrol on protein targets in nasopharyngeal carcinoma: Network pharmacology, molecular docking and experimental evaluations

Exploration of the effect of Celastrol on protein targets in nasopharyngeal carcinoma: Network pharmacology, molecular docking and experimental evaluations

Curcumol Inhibit Breast Cancer Growth Via NCL/ERα36 And PI3K/AKT Pathway

miRNAs as short non-coding RNAs in regulating doxorubicin resistance

Contact Info

Product

Resources

About