Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice

Amer, Maggie E.; Othman, Azza I.; Elsayed, Doaa A; El-Missiry, Mohamed A; Ammar, Omar A.

doi:10.1007/s11033-022-07315-2

Cited by 6 publications

(5 citation statements)

References 55 publications

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“…This finding mirrors those earlier findings that have examined the effect of SM nanocomposites on cancer cell viability. − ,− Recently, Amer et al reported that silymarin is able to induce cell cycle arrest at the sub-G1 phase and increase apoptosis in Ehrlich tumor cells through death receptor-related and mitochondrial pathways. In addition, they demonstrated that treatment of silymarin could lead to inhibition of angiogenesis and metastasis, characterized by upregulation of E-cadherin and downregulation of VEGF and NF-κB …”

Section: Discussionmentioning

confidence: 99%

“…In addition, they demonstrated that treatment of silymarin could lead to inhibition of angiogenesis and metastasis, characterized by upregulation of E-cadherin and downregulation of VEGF and NF-κB. 34 One unprecedented finding was that the cell treatment with the SM−tin(IV) complex could significantly restrict the colony formation ability of cells. This finding accords with a previous report, which showed that nanostructured silymarin composite reduces colonies formed by HT-29 cells.…”

Section: ■ Discussionmentioning

confidence: 99%

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Silymarin-Loaded Tin(IV) Nanoparticles Exhibit Enhanced Bioavailability and Antiproliferative Effects on Colorectal Cancer Cells

Abbasinia,

Heshmati,

Yousefi

et al. 2023

ACS Appl. Bio Mater.

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Silymarin (SM) exhibits potential therapeutic effects due to having antioxidant activity. However, the low solubility and bioavailability of SM restrict its biological performance. To overcome this limitation, this study aimed to develop a nanoformulation composed of SM and dimethyltindichloride and investigate the effect of SM-loaded Sn nanoparticles on cancer cell growth and survival. An SM−Sn complex was synthesized and then characterized using X-ray diffraction (XRD), transmission electron microscopy (TEM), Fourier transform infrared (FTIR), EDS-MAP, dynamic light scattering (DLS), and ζ-potential analysis. After that, the SW480 colorectal cancer cell line was treated with different concentrations of SM and the SM−Sn complex. Cell viability was examined through the 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, analyzing apoptosis, and live−dead assay. The lipid peroxidation rate was assessed through the measurement of thiobarbituric acid (TBA). Intracellular reactive oxygen species (ROS) level and cell population in the cell cycle were measured using a flow cytometry instrument. To evaluate the colonization ability of SW480 cells, a colony formation assay was performed. Gene expression analysis was also conducted using a real-time polymerase chain reaction (PCR) technique. The findings of this study revealed the effectiveness of the SM−Sn complex in decreasing SW480 cell viability by inducing cell death-associated mechanisms. We found that the SM−Sn complex increases intracellular ROS level and malondialdehyde (MDA) content. It was also revealed that the SM−Sn complex induces cell cycle arrest and the expression of apoptotic genes. In addition, the SM−Sn complex could effectively hinder SW480 cells from constituting colonies. We conclude that the use of tin(IV) as a scaffold for enhanced delivery of SM could be considered an efficient option for inhibiting cancer cell proliferation and survival.

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Section: Discussionmentioning

confidence: 99%

Section: ■ Discussionmentioning

confidence: 99%

Silymarin-Loaded Tin(IV) Nanoparticles Exhibit Enhanced Bioavailability and Antiproliferative Effects on Colorectal Cancer Cells

Abbasinia,

Heshmati,

Yousefi

et al. 2023

ACS Appl. Bio Mater.

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“…After 21 days of tumor induction, the animals were fasted for 12 h. Through cardiac puncture, blood was obtained for biochemical analyses while mice were under anesthesia using ketamine/xylazine (0.1 mL/100 g body weight, ip) (Amer et al, 2022). The plasma was separated using cold centrifugation and kept at −20°C.…”

Section: Methodsmentioning

confidence: 99%

“…Tumors were prepared for cell cycle analysis as described previously (Amer et al, 2022; Corver & Cornelisse, 2002). using RPMI 1640 medium for homogenization then filtered through fine mesh, and then centrifuged.…”

Section: Methodsmentioning

confidence: 99%

Selenium suppressed growth of Ehrlich solid tumor and improved health of tumor‐bearing mice

Hekal,

Amer,

Amer

et al. 2024

J Exp Zool Pt A

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Selenium (Se) is an important micronutritional biomolecule in cancer therapy. The current work evaluated the anticancer effect of Se and its ability to improve health of mice with solid Ehrlich carcinoma implanted subcutaneously. Four groups of five female BALB/c mice each were assembled. Ehrlich tumor cells were engrafted into two of them, either with or without Se therapy. The other groups served as control groups, either with or without Se treatment. Se treatment resulted in a notable decrease in both tumor volume and animal body mass in tumor‐bearing mice. Treatment with Se markedly increased oxidative stress in tumor while ameliorating oxidative stress in sera of tumors‐bearing mice. Similarly, treatment with Se resulted in downregulation of inflammatory cytokines (TNF‐α and IL‐6) while increasing IL‐10 in serum of tumor‐bearing mice. Conversely, selenium increased TNF‐ α and IL‐6 and decreased IL‐10 in tumor suggesting disruption of tumor immunity. The increased oxidative stress and inflammation in tumor tissue dysregulated cell cycle phases with increase apoptotic tumor cells population in G0/G1 phase. This is supported by the increased levels apoptotic regulating proteins (Bax and caspase‐3 and P‐53) while decreasing Bcl‐2 in the tumor tissue. Treatment with Se also resulted in increased comet parameters indicating DNA damage of tumor cells. Histopathological examination revealed a significant decrease in a number of neoplastic cells within tumor of mice that treated with Se. In conclusion, these findings suggest that Se therapy significantly suppressed solid tumor proliferation and growth while mitigating the health status of tumor‐bearing mice.

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“…Hepatocellular cellular carcinoma (HCC) is the sixth most common cancer in the world and the third leading cause of cancer deaths [2]. The etiology of liver cancer remains unclear with varied risk factors such as hepatitis, obesity, type 2 diabetes, nonalcoholic fatty liver disease, the lifestyle of the individuals (consumption of contaminated food with aflatoxin, heavy drinking of alcohol, ingestion of moldy foods, raw water drinking) and genetic predispositions [3].…”

Section: Introductionmentioning

confidence: 99%

Associations of methylene tetrahydrofolate reductase (MTHFR) polymorphism with hepatocellular carcinoma in Egyptian population

Abozeid,

Zaki,

Nagah

et al. 2024

Egypt Liver Journal

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Liver serves as a hub for key metabolic pathways such as folate cycle that provides one-carbon units for a network of metabolic reactions. Methylenetetrahydrofolate reductase (MTHFR) is a rate limiting enzyme in folate metabolism and thus it is vital for DNA methylation, synthesis and repair [1]. The objective of this study was to evaluate an eventual association between MTHFR polymorphisms C677T (rs1801133) and A1298C (rs1801131) and the susceptibility to hepatocellular carcinoma (HCC) in Egyptian population.Blood samples from patients and controls from Mansoura university hospital were used after signed consent and approval from Medical ethical committee. The two genetic loci were designed for amplification and genotyped by using PCR–RFLP.Our results clarify that, the most important predictors for HCC are T/T genotype of variant C677T and C/C genotype of variant (A1298C) with odds ratio 3.28 and 2.99 respectively. Also, MTHFR variant C677T genotype C/C or T/T combined with MTHFR variant A1298C genotype C/C were associated with an increased risk of HCC, with the OR, 2.6 and 7 respectively. CT genotype of MTHFR variant C677T showed significant difference between HCC grades and C allele of variant C677T showed significant difference in BCLC stages of HCC.Our data indicates that, the two variants (C677T and A1298C) constitute a risk factor for the development of HCC and this could be attributed to the low activities of the enzyme MTHFR that disturb one carbon metabolism and subsequently, DNA synthesis, repair and methylation, thus cellular redox state, growth, and proliferation.

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Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice

Cited by 6 publications

References 55 publications

Silymarin-Loaded Tin(IV) Nanoparticles Exhibit Enhanced Bioavailability and Antiproliferative Effects on Colorectal Cancer Cells

Silymarin-Loaded Tin(IV) Nanoparticles Exhibit Enhanced Bioavailability and Antiproliferative Effects on Colorectal Cancer Cells

Selenium suppressed growth of Ehrlich solid tumor and improved health of tumor‐bearing mice

Associations of methylene tetrahydrofolate reductase (MTHFR) polymorphism with hepatocellular carcinoma in Egyptian population

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