Dandelion root extract affects ESCC progression<i>via</i>regulating multiple signal pathways

Duan, Xiaofang; Pan, Limin; Deng, Yuying; Liu, Ya; Han, Xue; Han, Fangfang; Li, Yuxi; Li, Ming; Wang, Tianxiao

doi:10.1039/d1fo01093j

Cited by 6 publications

(4 citation statements)

References 32 publications

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“…Other treatments, including immune checkpoint inhibitors, tumor vaccines, and epigenetic-targeted therapy, remain in progress 41 , 43 . Furthermore, in preclinical and clinical studies, using natural substrates isolated from medicinal plants has obtained promising outcomes for ESCC 44 – 47 ; however, further assessment of the clinical application is time-consuming and is still ongoing. The application of FDA-approved drugs for cancer treatment has been a hotspot for studying pharmacokinetics, establishing safety in humans, and evaluating toxicity 31 , 32 .…”

Section: Discussionmentioning

confidence: 99%

Dexrazoxane inhibits the growth of esophageal squamous cell carcinoma by attenuating SDCBP/MDA-9/syntenin-mediated EGFR-PI3K-Akt pathway activation

Du,

Xiao,

Han

et al. 2024

Sci Rep

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Syndecan-binding protein (SDCBP) was reported to stimulate the advancement of esophageal squamous cell carcinoma (ESCC) and could potentially be a target for ESCC treatment. There is a growing corpus of research on the anti-tumor effects of iron chelators; however, very few studies have addressed the involvement of dexrazoxane in cancer. In this study, structure-based virtual screening was employed to select drugs targeting SDCBP from the Food and Drug Administration (FDA)-approved drug databases. The sepharose 4B beads pull-down assay revealed that dexrazoxane targeted SDCBP by interacting with its PDZ1 domain. Additionally, dexrazoxane inhibited ESCC cell proliferation and anchorage-independent colony formation via SDCBP. ESCC cell apoptosis and G2 phase arrest were induced as measured by the flow cytometry assay. Subsequent research revealed that dexrazoxane attenuated the binding ability between SDCBP and EGFR in an immunoprecipitation assay. Furthermore, dexrazoxane impaired EGFR membrane localization and inactivated the EGFR/PI3K/Akt pathway. In vivo, xenograft mouse experiments indicated that dexrazoxane suppressed ESCC tumor growth. These data indicate that dexrazoxane might be established as a potential anti-cancer agent in ESCC by targeting SDCBP.

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Section: Discussionmentioning

confidence: 99%

Dexrazoxane inhibits the growth of esophageal squamous cell carcinoma by attenuating SDCBP/MDA-9/syntenin-mediated EGFR-PI3K-Akt pathway activation

Du,

Xiao,

Han

et al. 2024

Sci Rep

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“…The 24-well transwell chambers (pore size, 8 μm; Corning Incorporated, Corning, NY, United States)need to be covered with or without Matrigel matrix (BD Biosciences, CA, United States) for invasion or migration. Please refer to the literature for specific method ( Duan et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

“…Previous researches have shown that dandelion exhibits anti-inflammatory and anti-cancer effects. Moreover, our previous study has shown that Dandelion root extract (DRE) significantly inhibited the growth and migration of ESCC ( Duan et al, 2021 ). Likewise, dandelion seed has the function of antibacterial and anti-inflammatory, liver and gallbladder protection, body immunity enhancement, but its role in tumor has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Dandelion Seed Extract Affects Tumor Progression and Enhances the Sensitivity of Cisplatin in Esophageal Squamous Cell Carcinoma

Deng

Zhang

et al. 2022

Front. Pharmacol.

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Like dandelion, dandelion seed also have anti-inflammatory activity. Therefore, in this article, we intend to explore the anti-cancer availability of aqueous dandelion seed extract (DSE) in esophageal squamous cell carcinoma (ESCC). Firstly, the effects of DSE on cell proliferation, apoptosis, migration, invasion and angiogenesis were investigated. Then to explore the mechanism of DSE against ESCC, the levels of proliferation-associated proteins (PI3K, Akt and pAkt), apoptosis-associated proteins (survivin, Bcl-2, Bax, caspase3 and caspase9), metastasis-associated proteins (MMP2, MMP9, VEGF) and EMT progression-associated proteins (Snail, E-cadherin and Vimentin) were analyzed. Next, we further explored the effect of DSE on the sensitivity of cisplatin (DDP) in ESCC cells and investigated the effect of DSE combined with DDP on DNA damage repair-associated proteins (MSH2, MLH1 and ERCC1) and drug resistant target protein STAT3. The results indicated that DSE selectively inhibited cell growth, proliferation, migration, invasion, angiogenesis and induced cell apoptosis in ESCC cells. It was observed the decreased PI3K, Akt and pAkt proteins levels in KYSE450 and Eca109 cells administrated with DSE. The data also showed that the application of DSE decreased the level of survivin and the ratio of Bcl-2/Bax, while increased the levels of caspase3 and caspase9. We also observed that DSE significantly decreased the levels of MMP2, MMP9 and VEGF proteins and inhibited the EMT progression in KYSE450 and Eca109 cells. In addition, survivin plays a critical role in DSE against ESCC followed with the application of survivin inhibitor YM155 impairing the inhibitory abilities of DSE in ESCC cells. Meanwhile, it was observed that DSE enhances the sensitivity of DDP to human ESCC cells via promoting DNA damage and inhibiting phosphorylation of STAT3. Therefore, DSE may affect ESCC progression and enhance the sensitivity of cisplatin, and consequently become an effective anti-cancer option for human ESCC treatment.

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“…Dandelion, termed Taraxacum mongolicum , had been used as a classical herbal medicine based on the traditional Chinese medicine theory in treating mammary diseases, including mammary abscess and hyperplasia of mammary glands ( Martinez et al, 2015 ). Sizeable evidence indicated that dandelion and its components have significant inhibitory effects against various tumor cells ( Gauhar et al, 2017 ; Zhu et al, 2017 ; Duan et al, 2021 )and lipids regulatory impact on normal cells and fat animal models, which is closely related to activating the AMP-activated protein kinase (AMPK) pathway ( Liu et al, 2014 ; Gauhar et al, 2017 ). For example, dandelion extract significantly reduced adipogenesis and lipid accumulation in 3T3-L1 ( González-Castejón et al, 2013 ), as well as decreased serum levels of cholesterol and triglyceride and liver lipid accumulation in high-fat-fed rabbits ( Choi et al, 2010 ) and rats ( Davaatseren et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Dandelion extract inhibits triple-negative breast cancer cell proliferation by interfering with glycerophospholipids and unsaturated fatty acids metabolism

et al. 2022

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Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype with limited treatment options and a poor prognosis. TNBC exists widely reprogrammed lipid metabolism, and its metabolic-associated proteins and oncometabolites are promising as potential therapeutic targets. Dandelion (Taraxacum mongolicum) is a classical herbal medicine used to treat breast diseases based on traditional Chinese medicine theory and was reported to have antitumor effects and lipid regulatory capacities. Our previous study showed that dandelion extract was effective against TNBC. However, whether dandelion extract could regulate the lipid metabolisms of TNBC and exert its antitumor effects via interfering with lipids metabolism remained unclear. In this study, an integrated approach combined with network pharmacology and multi-omics techniques (including proteomics, metabolomics, and lipidomics) was performed to investigate the potential regulatory mechanisms of dandelion extract against TNBC. We first determined the antitumor effects of dandelion extract in vitro and in vivo. Then, network pharmacology analysis speculated the antitumor effects involving various metabolic processes, and the multi-omics results of the cells, tumor tissues, and plasma revealed the changes in the metabolites and metabolic-associated proteins after dandelion extract treatment. The alteration of glycerophospholipids and unsaturated fatty acids were the most remarkable types of metabolites. Therefore, the metabolism of glycerophospholipids and unsaturated fatty acids, and their corresponding proteins CHKA and FADS2, were considered the primary regulatory pathways and biomarkers of dandelion extract against TNBC. Subsequently, experimental validation showed that dandelion extract decreased CHKA expression, leading to the inhibition of the PI3K/AKT pathway and its downstream targets, SREBP and FADS2. Finally, the molecular docking simulation suggested that picrasinoside F and luteolin in dandelion extract had the most highly binding scores with CHKA, indicating they may be the potential CHKA inhibitors to regulate glycerophospholipids metabolisms of TNBC. In conclusion, we confirmed the antitumor effects of dandelion extract against TNBC cells in vitro and demonstrated that dandelion extract could interfere with glycerophospholipids and unsaturated fatty acids metabolism via downregulating the CHKA expression and inhibiting PI3K/AKT/SREBP/FADS2 axis.

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Dandelion root extract affects ESCC progressionviaregulating multiple signal pathways

Abstract: Dandelion, a medicinal and edible plant, exhibits anti-inflammatory activity. The purpose of the present study was to investigate the inhibitory effectiveness of aqueous dandelion root extract (DRE) on esophageal squamous...

Cited by 6 publications

References 32 publications

Dexrazoxane inhibits the growth of esophageal squamous cell carcinoma by attenuating SDCBP/MDA-9/syntenin-mediated EGFR-PI3K-Akt pathway activation

Dexrazoxane inhibits the growth of esophageal squamous cell carcinoma by attenuating SDCBP/MDA-9/syntenin-mediated EGFR-PI3K-Akt pathway activation

Dandelion Seed Extract Affects Tumor Progression and Enhances the Sensitivity of Cisplatin in Esophageal Squamous Cell Carcinoma

Dandelion extract inhibits triple-negative breast cancer cell proliferation by interfering with glycerophospholipids and unsaturated fatty acids metabolism

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