Antitumor Activity of Luteolin Against Ehrlich Solid Carcinoma in Rats via Blocking Wnt/β-Catenin/SMAD4 Pathway

Aljohani, Heba; Khodier, Ahmed E; Al-Gayyar, Mohammed M

doi:10.7759/cureus.39789

Cited by 9 publications

(7 citation statements)

References 19 publications

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“…In YQQYJDF, the core active ingredients corresponding to these five target genes are luteolin, quercetin, kaempferol and stigmasterol. Luteolin is a natural flavone compound that is considered to have antitumor effects [ 37 , 38 ]. Some studies have confirmed that luteolin can significantly inhibit glioma cell proliferation, migration, and invasion and induce their apoptosis [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology -based study on the mechanism of traditional Chinese medicine in the treatment of glioblastoma multiforme

Liang,

Zhang,

et al. 2023

BMC Complement Med Ther

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Background Glioblastoma multiforme (GBM) is one of the most common primary malignant brain tumors. Yi Qi Qu Yu Jie Du Fang (YYQQJDF) is a traditional Chinese medicine (TCM) prescription for GBM. The present study aimed to use a network pharmacology method to analyze the underlying mechanism of YQQYJDF in treating GBM. Methods GBM sample data, active ingredients and potential targets of YQQYJDF were obtained from databases. R language was used to screen differentially expressed genes (DEGs) between GBM tissues and normal tissues, and to perform enrichment analysis and weighted gene coexpression network analysis (WGCNA). The Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database was used to perform a protein‒protein interaction (PPI) analysis. A Venn diagram was used to obtain the core target genes of YQQYJDF for GBM treatment. Molecular docking was used to verify the binding between the active ingredient molecules and the proteins corresponding to the core target genes. Cell proliferation assays and invasion assays were used to verify the effect of active ingredients on the proliferation and invasion of glioma cells. Results A total of 73 potential targets of YQQYJDF in the treatment of GBM were obtained. Enrichment analyses showed that the biological processes and molecular functions involved in these target genes were related to the activation of the G protein-coupled receptor (GPCR) signaling pathway and the regulation of hypoxia. The neuroactive ligand‒receptor pathway, the cellular senescence pathway, the calcium signaling pathway, the cell cycle pathway and the p53 signaling pathway might play important roles. Combining the results of WGCNA and PPI analysis, five core target genes and their corresponding four core active ingredients were screened. Molecular docking indicated that the core active ingredient molecules and the proteins corresponding to the core target genes had strong binding affinities. Cell proliferation and invasion assays showed that the core active ingredients of YQQYJDF significantly inhibited the proliferation and invasion of glioma cells (P < 0.01). Conclusions The present study predicted the possible active ingredients and targets of YQQYJDF in treating GBM, and analyzed its possible mechanism. These results may provide a basis and ideas for further research.

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Section: Discussionmentioning

confidence: 99%

Network pharmacology -based study on the mechanism of traditional Chinese medicine in the treatment of glioblastoma multiforme

Liang,

Zhang,

et al. 2023

BMC Complement Med Ther

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“…Rats were subjected to intramuscular injection of 0.15 ml Ehrlich cells (2×10 6 ) in the thigh of the left hind leg [9,10].…”

Section: Esc Groupmentioning

confidence: 99%

Antitumor Activity of Ferulic Acid Against Ehrlich Solid Carcinoma in Rats via Affecting Hypoxia, Oxidative Stress and Cell Proliferation

Alghamdi,

Khalifah,

Alhawati

et al. 2023

Cureus

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BackgroundFerulic acid is a natural compound commonly found in fruits and vegetables like tomatoes, sweet corn, rice bran, and dong quai. It has various beneficial effects on the body, such as anti-inflammatory, anti-apoptotic, hepatoprotective, cardioprotective, and neuroprotective properties. AimsWe conducted a study to investigate the antitumor activity of ferulic acid against Ehrlich solid carcinoma (ESC), specifically by affecting hypoxia-inducible factor (HIF)-1α and its subsequent effects on other factors like nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), cellular Myc (cMyc), cyclin D1, mammalian target of rapamycin (mTOR), and signal transducer and activator of transcription 3 (STAT3). Materials and methodsThe study involved implanting rats with ESC cells and administering 50 mg/kg of ferulic acid orally daily for eight days. Sections of the muscles with ESC were stained with toluidine blue or immunostained with anti-HIF-1α antibodies. The tumor samples were used to evaluate the expression of HIF-1α, Nrf2, HO-1, cMyc, cyclin D1, mTOR, and STAT3. ResultsFerulic acid increased mean survival time, reduced tumor volume and weight, and improved the appearance of the tumor tissue. Furthermore, ferulic acid significantly elevated the expression of Nrf2 and HO-1, while reducing the expression of HIF-1α, Nrf2, HO-1, cMyc, cyclin D1, mTOR, and STAT3. ConclusionsFerulic acid can reduce tumor size and weight while improving the structure of muscle cells, suggesting it may have antineoplastic activity against ESC. Further investigation revealed that ferulic acid downregulates HIF-1α, increasing the expression of antioxidant proteins Nrf2 and HO-1. Additionally, ferulic acid decreases the expression of proliferation markers cMyc and cyclin D1 and downregulates cellular regulators mTOR and STAT3.Categories: Oncology Keywords: signal transducer and activator of transcription 3 (stat3), nuclear factor erythroid 2-related factor 2 (nrf2), mammalian target of rapamycin (mtor), hypoxia-inducible factor (hif)-1α, heme oxygenase-1 (ho-1), ehrlich solid carcinoma (esc), cyclin d1, cellular myc (cmyc)

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“…During the experiment period, the control group did not receive any treatment. In contrast, the ESC group was given an intramuscular injection of 0.15 mL 2×10 6 Ehrlich cells in the thigh of the left hind leg [7][8][9]. In the ESC group treated with arctiin, we induced ESC in rats.…”

Section: Animals' Treatmentmentioning

confidence: 99%

Arctiin Inhibits Inflammation, Fibrosis, and Tumor Cell Migration in Rats With Ehrlich Solid Carcinoma

Alfair,

Jabarti,

Albalawi

et al. 2023

Cureus

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Background and objectives: ESC or Ehrlich solid carcinoma is a type of tumor originating from a spontaneous mammary adenocarcinoma in mice. It is a highly aggressive and fast-growing carcinoma that can create a solid mass when inserted under the skin. Its solid, undifferentiated form makes it an ideal model for researching cancer biology, tumor immunology, and testing various anti-cancer treatments. Additionally, arctiin has multiple beneficial properties, such as anti-proliferative, anti-oxidative, anti-adipogenic, and anti-bacterial. This study aimed to explore the potential anti-cancer benefits of arctiin in rats with ESC while also analyzing its effects on cell fibrosis markers, tumor cell migration, and inflammasome pathways. Methods: Rats were given a tumor in their left hind limb via an intramuscular injection consisting of 2×10 6 cells. After eight days, some of the rats received a daily oral dose of 30 mg/kg of arctiin for three weeks. Muscle samples were observed under an electron microscope or stained with hematoxylin/eosin. Additionally, gene expression and protein levels of toll-like receptor 4 (TLR4), NLR family pyrin domain containing 3 (NLRP3), signal transducer and activator of transcription 3 (STAT3), transforming growth factor (TGF)-β, endothelial growth factor (VEGF), and cyclin D1 were assessed in another part of the muscle samples. Results: When ESC rats were given arctiin as a treatment, their mean survival time increased and their tumor volume and weight decreased. Additionally, when tumor tissue was examined under an electron microscope, it showed signs of pleomorphic cells, necrosis, nuclear fragmentation, membrane damage with cytoplasmic content spilling, and loss of cellular junction. The stained sections with hematoxylin/eosin showed a dense cellular mass and compressed, degenerated, and atrophied muscle. However, treatment with arctiin improved all these effects. Finally, the expression of TLR4, NLRP3, STAT3, TGF-β, VEGF, and cyclin D1 was significantly reduced with arctiin treatment. Conclusions: Through the use of arctiin, tumor size and weight were effectively reduced, leading to an increase in the average survival time of rats and an improvement in muscle structure. Additional research has shown that arctiin is able to suppress inflammation, fibrosis, and the migration of tumor cells by inhibiting STAT3, TGF-β1, TLR4, NLRP3, VEGF, and cyclin D1.

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Antitumor Activity of Luteolin Against Ehrlich Solid Carcinoma in Rats via Blocking Wnt/β-Catenin/SMAD4 Pathway

Cited by 9 publications

References 19 publications

Network pharmacology -based study on the mechanism of traditional Chinese medicine in the treatment of glioblastoma multiforme

Network pharmacology -based study on the mechanism of traditional Chinese medicine in the treatment of glioblastoma multiforme

Antitumor Activity of Ferulic Acid Against Ehrlich Solid Carcinoma in Rats via Affecting Hypoxia, Oxidative Stress and Cell Proliferation

Arctiin Inhibits Inflammation, Fibrosis, and Tumor Cell Migration in Rats With Ehrlich Solid Carcinoma

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