New phosphorus ylide palladacyclic: Synthesis, characterization, X-Ray crystal structure, biomolecular interaction studies, molecular docking and in vitro cytotoxicity evaluations

Karami, Kazem; Rahimi, Mahzad; Zakariazadeh, Mostafa; Büyükgüngör, Orhan; Amirghofran, Zahra

doi:10.1016/j.jorganchem.2018.09.018

Cited by 18 publications

(5 citation statements)

References 77 publications

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“…100 runs were considered for molecular docking of DNA with Ax. Default values for Auto Dock Tools parameters were considered, and the Lamarckian genetic algorithm mode was set on molecular docking simulation [24,25].…”

Section: Molecular Dockingmentioning

confidence: 99%

Astaxanthin Binding Affinity to DNA: Studied By Fluorescence, Surface Plasmon Resonance and Molecular Docking Methods

et al. 2023

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Astaxanthin (Ax), as a novel food supplement, a pink-red pigment, belongs to the carotenoid family. The study of DNA interactions with various drugs is very important for estimating the mechanism of interaction and developing new drugs. The purpose of this study is to investigate the binding a nity of Ax to double strand (ds) DNA evaluated by using a uorescence spectroscopy, surface plasmon resonance (SPR) and docking approaches. The uorescence results shown that Ax can quench the intensity amount of DNA uorescence via a static quenching way. In the SPR method, DNA molecules were attached on a gold sensor surface. Using different amounts of ds DNA, the kinetic values K D , K A , and K a were calculated. The obtained nding con rm that the binding of Ax to DNA has an exothermic and spontaneous mechanism. Also, thermodynamic studies were carried out using uorescence analysis at four different temperatures, and the resulted negative data for ΔH and ΔS displayed that the main binding strength in the interaction of Ax to DNA was hydrogen bonding. Molecular docking results con rmed that the side chains of Ax interact speci cally with base pairs and the DNA backbone. HighlightsThe binding strength of astaxanthin (Ax) to double strands (ds) DNA was investigated.The uorescence results shown that Ax can quench the DNA.The obtained negative values for ΔH and ΔS indicated that the binding of Ax to DNA was spontaneous process.Major binding force involved in intercalation of AX to DNA was hydrogen bonding.Molecular docking results con rmed that the side chains of Ax interact with DNA.

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Section: Molecular Dockingmentioning

confidence: 99%

Astaxanthin Binding Affinity to DNA: Studied By Fluorescence, Surface Plasmon Resonance and Molecular Docking Methods

et al. 2023

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“…The effect of CD133 + HPCs on the proliferation of breast cancer cells was quantified by 3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays [20]. We co-cultured MCF-7 or MDA-MB-231 cells (2 × 10 3 cells/well) with or without (blank control), CD133 + HPCs and CD133-HUCBCs at a ratio of 20:1 in triplicate in 96-well plates for 24-120 h. We quantified the viability of individual wells by MTT.…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Human CD133-Positive Hematopoietic Progenitor Cells Enhance the Malignancy of Breast Cancer Cells

Zhang

Qinglian

Liu

et al. 2020

Preprint

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Background: Human CD133 + hematopoietic progenitor cells (HPCs) are a specific subset of cells and can regulate the malignancy of tumors. However, how CD133 + HPCs affect the malignancy of human breast cancer has not been clarified.Methods: The CD133 + HPCs were isolated and purified from human umbilical cord blood (UCB) .We used in vitro culture of the MCF-7 and MDA-MB-231 cell line, and MCF-7 and MDA-MB-231 cells into nude mice in order to tested whether CD133 + HPCs affected the apoptosis, proliferation, invasion and EMT of breast cancer cells.Results: Co-culture with CD133 + HPCs, but not UCB CD133- cells, promoted the proliferation of human breast cancer MCF-7 or MDA-MB-231 cells, accompanied by reducing their spontaneous apoptosis in vitro and co-administration with CD133 + HPCs significantly enhanced the growth of implanted breast cancer in vivo. Furthermore, co-culture with CD133 + HPCs, enhanced the invasion of breast cancer cells, N-cadherin and Vimentin expression, but reduced E-cadherin expression in Breast cancer cells.Conclusions: The data indicated that CD133 + HPCs enhanced the malignancy of breast cancer cells by inhibiting their spontaneous apoptosis and promoting the process of epithelial mesenchymal transition. These findings may provide new insights in the role of human CD133 + HPCs in the pathogenic process of breast cancer. Therefore, CD133 + HPCs may be a new therapeutic target for inhibiting the progression of breast cancer.

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“…However, few experiments have addressed the role of HPCs in breast cancer. Furthermore, clinical studies indicate that transplantation with hematopoietic stem cells after high dose of chemotherapies benefits patients with advanced breast cancer [ 22 , 23 ]. However, there is little information on how human HPCs regulate the malignancy of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Human CD133-positive hematopoietic progenitor cells enhance the malignancy of breast cancer cells

et al. 2020

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Background Human CD133+ hematopoietic progenitor cells (HPCs) are a specific subset of cells that can regulate tumor malignancy. However, the mechanism by which CD133+ HPCs affect the malignancy of human breast cancer has not been reported. Methods CD133+ HPCs were isolated and purified from human umbilical cord blood (UCB). We used in vitro culture of MCF-7 and MDA-MB-231 cell lines, and MCF-7 and MDA-MB-231 cells in nude mice to evaluate whether CD133+ HPCs affected the apoptosis, proliferation, invasion and epithelial mesenchymal transition EMT of breast cancer cells. Results Co-culture with CD133+ HPCs, but not UCB CD133- cells, promoted the proliferation of human breast cancer MCF-7 and MDA-MB-231 cells, accompanied by reducing in vitro spontaneous apoptosis. Co-administration of these two lines with CD133+ HPCs significantly enhanced the growth of implanted breast cancer in vivo. Furthermore, co-culture with CD133+ HPCs, enhanced the invasion of breast cancer cells, N-cadherin and Vimentin expression, but reduced E-cadherin expression in breast cancer cells. Conclusions Our study demonstrated that CD133+ HPCs enhance the malignancy of breast cancer cells by attenuating spontaneous apoptosis and promoting the process of epithelial mesenchymal transition. These findings may provide new insights into the role of human CD133+ HPCs in breast cancer pathogenesis. Therefore, CD133+ HPCs may be a new therapeutic target for inhibiting the progression of breast cancer.

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New phosphorus ylide palladacyclic: Synthesis, characterization, X-Ray crystal structure, biomolecular interaction studies, molecular docking and in vitro cytotoxicity evaluations

Cited by 18 publications

References 77 publications

Astaxanthin Binding Affinity to DNA: Studied By Fluorescence, Surface Plasmon Resonance and Molecular Docking Methods

Astaxanthin Binding Affinity to DNA: Studied By Fluorescence, Surface Plasmon Resonance and Molecular Docking Methods

Human CD133-Positive Hematopoietic Progenitor Cells Enhance the Malignancy of Breast Cancer Cells

Human CD133-positive hematopoietic progenitor cells enhance the malignancy of breast cancer cells

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