Cytotoxicity of isoflavones and biflavonoids from Ormocarpum kirkii towards multi-factorial drug resistant cancer

Adem, Fozia A.; Mbaveng, Armelle T.; Kuete, Victor; Heydenreich, Matthias; Ndakala, Albert; Irungu, Beatrice; Yenesew, Abiy; Efferth, Thomas

doi:10.1016/j.phymed.2019.152853

Cited by 50 publications

(31 citation statements)

References 48 publications

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“…β-elemene, isolated from Curcuma zedoaria Roscoe, was shown to enhance the sensitivity of lung cancer cells to cisplatin by increasing intracellular ROS levels and decreasing cytoplasmic glutathione amounts [119]. Isoflavones and biflavonoids from Ormocarpum kirkii were reported to induce apoptosis in multiple chemoresistant carcinoma cells through enhanced ROS generation [120]. Phillygenin is a plant-derived tetrahydrofurofuran lignan.…”

Section: Other Related Metabolismsmentioning

confidence: 99%

Targeting Cancer Metabolism to Resensitize Chemotherapy: Potential Development of Cancer Chemosensitizers from Traditional Chinese Medicines

Guo

Tan

Chen

et al. 2020

Cancers

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Cancer is a common and complex disease with high incidence and mortality rates, which causes a severe public health problem worldwide. As one of the standard therapeutic approaches for cancer therapy, the prognosis and outcome of chemotherapy are still far from satisfactory due to the severe side effects and increasingly acquired resistance. The development of novel and effective treatment strategies to overcome chemoresistance is urgent for cancer therapy. Metabolic reprogramming is one of the hallmarks of cancer. Cancer cells could rewire metabolic pathways to facilitate tumorigenesis, tumor progression, and metastasis, as well as chemoresistance. The metabolic reprogramming may serve as a promising therapeutic strategy and rekindle the research enthusiasm for overcoming chemoresistance. This review focuses on emerging mechanisms underlying rewired metabolic pathways for cancer chemoresistance in terms of glucose and energy, lipid, amino acid, and nucleotide metabolisms, as well as other related metabolisms. In particular, we highlight the potential of traditional Chinese medicine as a chemosensitizer for cancer chemotherapy from the metabolic perspective. The perspectives of metabolic targeting to chemoresistance are also discussed. In conclusion, the elucidation of the underlying metabolic reprogramming mechanisms by which cancer cells develop chemoresistance and traditional Chinese medicines resensitize chemotherapy would provide us a new insight into developing promising therapeutics and scientific evidence for clinical use of traditional Chinese medicine as a chemosensitizer for cancer therapy.

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Section: Other Related Metabolismsmentioning

confidence: 99%

Targeting Cancer Metabolism to Resensitize Chemotherapy: Potential Development of Cancer Chemosensitizers from Traditional Chinese Medicines

Guo

Tan

Chen

et al. 2020

Cancers

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“…The cytotoxicity of botanicals (ASL, ASLa-ASLc), phytochemicals (1-6) and doxorubicin was determined using the well-described resazurin reduction assay (RRA) [20,21] at identical experimental conditions as documented earlier [22,23]. After 72 h incubation in the standard culture condition (humidified 5% CO 2 atmosphere at 37 C), the fluorescence was measured with Infinite M2000 Pro™ plate reader (Tecan, Crailsheim, Germany) at 544 nm as excitation wavelength and 590 nm as detection wavelength.…”

Section: Cytotoxicity Assaymentioning

confidence: 99%

“…The distribution of cycle phases of CCRF-CEM cells after application of the crude extract (ASL) or doxorubicin was analyzed by the flow cytometry [25,26]. We followed the methods of Mbaveng et al [23]. Additionally, flow cytometry was also applied with annexin V/propidium iodide (PI) staining to detect apoptotic cells as previously described [25,26].…”

Section: Analysis Of Cell Cycle Distribution and Detection Of Apoptotic Cells By Flow Cytometrymentioning

confidence: 99%

“…After application of ASL to the cells, followed by 6 h incubation under standard culture conditions, the activities of caspases were evaluated using Caspase-Glo 3/7, 8 and 9 Assay kits (Promega, Mannheim, Germany) with an Infinite M2000 ProTM plate reader (Tecan) as previously reported [19]. The protocol was followed as described by Mbaveng et al [23].…”

Section: Detection Of Caspases Activationmentioning

confidence: 99%

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Botanicals from the leaves of Acacia sieberiana had better cytotoxic effects than isolated phytochemicals towards MDR cancer cells lines

Ngaffo

Tchangna

Mbaveng

et al. 2020

Heliyon

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The efficiency of cancer chemotherapy is seriously hampered by the development of resistance of neoplastic cells to cytotoxic agents. In the present investigation, the cytotoxicity of the dichloromethane-methanol (1:1) extract of Acacia sieberiana (ASL), fractions (ASLa-c) from the leaves and isolated compounds: chrysoeriol 5) and luteolin (6) was investigated. The study was extended to the assessment of the mode of induction of apoptosis by ASL. The resazurin reduction assay (RRA) was used for cytotoxicity studies. Assessments of cell cycle distribution, apoptosis, and reactive oxygen species (ROS) were performed by flow cytometry. A caspase-Glo assay was used to evaluate caspase activities. Botanicals ASL, ASLb and ASLc as well as doxorubicin displayed observable IC 50 values towards the nine tested cancer cell lines while ASLa and compounds 1-7 had selective activities. The IC 50 values ranged from 13.45 μg/mL (in CCRF-CEM leukemia cells) to 33.20 μg/mL (against MDA-MB-231-BCRP breast adenocarcinoma cells) for ASL, from 16.42 μg/mL (in CCRF-CEM cells) to 29.64 μg/mL (against MDA-MB-231-pcDNA cells) for ASLc, and from 22.94 μg/mL (in MDA-MB-231-BCRP cells) to 40.19 μg/mL (against HCT116 (p53À/À) colon adenocarcinoma cells) for ASLb (Table 1), and from 0.02 μM (against CCRF-CEM cells) to 122.96 μM (against CEM/ADR5000 cells) for doxorubicin. ASL induced apoptosis in CCRF-CEM cells, mediated by ROS production. Acacia sieberiana is a good cytotoxic plant and should be further explored to develop an anticancer phytomedicine to combat both sensitive and drug resistant phenotypes.

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“…In addition, numerous botanicals and phytochemicals derived from African medicinal plants have been found active against MDR cancer cell lines [ 7 , 8 ]. Some of such prominent phytochemicals include terpenoids: salvimulticanol and candesalvone B methyl ester [ 9 ], epunctanone [ 10 ], and ardisiacrispin B [ 11 ], phenolics: 2-acetyl-7-methoxynaphtho [2,3-b]furan-4,9-quinone [ 12 ], 6 α -hydroxyphaseollidin [ 13 ], licoagrochalcone A [ 14 ], 7-dihydroxy-4′-methoxy-6,8-diprenylisoflavone, and 7,7″-di- O -methylchamaejasmin [ 15 ], and alkaloids: 1,3-dimethoxy-10-methylacridone [ 16 ], isotetrandrine [ 17 ], and ungeremine [ 18 ]. However, more hit compounds should be identified to increase our arsenal of cytotoxic compounds and to secure better the chances of later obtaining new clinically usable molecules.…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic Constituents of the Bark of Hypericum roeperianum towards Multidrug‐Resistant Cancer Cells

Guefack

Damen

Mbaveng

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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The global cancer burden remains a serious concern with the alarming incidence of one in eight men and one in eleven women dying in developing countries. This situation is aggravated by the multidrug resistance (MDR) of cancer cells that hampers chemotherapy. In this study, the cytotoxicity of the methanol extract (HRB), fractions (HRBa, HRBb, and HRBa1-5), and compounds from the bark of Hypericum roeperianum (HRB) was evaluated towards a panel of 9 cancer cell lines. The mode of action of the HRB and trichadonic acid (1) was also studied. Column chromatography was applied to isolate the constituents of HRB. The cytotoxicity of botanicals and phytochemicals was evaluated by the resazurin reduction assay (RRA). Caspase-Glo assay was used to evaluate the activity of caspases, and reactive oxygen species (ROS) (H2DCFH-DA) were assessed by flow cytometry. Phytochemicals isolated from HRB were trichadonic acid (1), fridelan-3-one (2), 2-hydroxy-5-methoxyxanthone (3), norathyriol (4), 1,3,5,6-tetrahydroxyxanthone (5), betulinic acid (6), 3′-hydroxymethyl-2′-(4″-hydroxy-3″,5″-dimethoxyphenyl)-5′,6′:5,6-(6,8-dihydroxyxanthone)-1′,4′-dioxane (7), and 3′-hydroxymethyl-2′-(4″-hydroxy-3″,5″-dimethoxyphenyl)-5′,6′:5,6-(xanthone)-1′,4′-dioxane (8). Botanicals HRB, HRBa, HRBa2-4, HRBb, and doxorubicin displayed cytotoxic effects towards the 9 tested cancer cell lines. The recorded IC50 values ranged from 11.43 µg/mL (against the P-glycoprotein (gp)-overexpressing CEM/ADR5000 leukemia cells) to 26.75 µg/mL (against HCT116 (p53+/+) colon adenocarcinoma cells) for the crude extract HRB. Compounds 1, 5, and doxorubicin displayed cytotoxic effects towards the 9 tested cancer cell lines with IC50 values varying from 14.44 µM (against CCRF-CEM leukemia cells) to 44.20 µM (against the resistant HCT116 (p53−/−) cells) for 1 and from 38.46 µM (against CEM/ADR5000 cells) to 112.27 µM (against the resistant HCT116 (p53−/−) cells) for 5. HRB and compound 1 induced apoptosis in CCRF-CEM cells. The apoptotic process was mediated by enhanced ROS production for HRB or via caspases activation and enhanced ROS production for compound 1. This study demonstrated that Hypericum roeperianum is a potential source of cytotoxic phytochemicals such as trichadonic acid and could be further exploited in cancer chemotherapy.

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Cytotoxicity of isoflavones and biflavonoids from Ormocarpum kirkii towards multi-factorial drug resistant cancer

Cited by 50 publications

References 48 publications

Targeting Cancer Metabolism to Resensitize Chemotherapy: Potential Development of Cancer Chemosensitizers from Traditional Chinese Medicines

Targeting Cancer Metabolism to Resensitize Chemotherapy: Potential Development of Cancer Chemosensitizers from Traditional Chinese Medicines

Botanicals from the leaves of Acacia sieberiana had better cytotoxic effects than isolated phytochemicals towards MDR cancer cells lines

Cytotoxic Constituents of the Bark of Hypericum roeperianum towards Multidrug‐Resistant Cancer Cells

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