Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

Tolomeo, Manlio; Grimaudo, Stefania; Cristina, Antonietta Di; Pipitone, Rosaria Maria; Dusonchet, Luisa; Meli, Maria; Crosta, Lucia; Gebbia, Nicola; Invidiata, Francesco Paolo; Titone, Lucina; Daniele, Simona

doi:10.1016/j.canlet.2008.02.025

Cited by 68 publications

(43 citation statements)

References 26 publications

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“…As per available report, it is suggested that galangin suppresses the b-catenin regulated transcription in case of liver cancers (JungSug et al 2011). Galangin disrupts cell division of cancer cells at the G 0 -G 1 phase of cell cycle and it is also a strong inhibitor of Hs578T cell proliferation (Tolomeo et al 2008). Our results revealed that galangin demonstrated maximum antineoplastic effects against Sarcoma 180 and are in agreement with earlier reported results (Murray et al 2006).…”

Section: Discussionsupporting

confidence: 93%

Flavonoids from Heliotropium subulatum exudate and their evaluation for antioxidant, antineoplastic and cytotoxic activities II

2016

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The flavonoids are the largest group of phenolic compounds isolated from a wide range of higher plants. These compounds work as antimicrobials, anti-insect agents and protect plants from other types of biotic and abiotic stresses. Various researchers have suggested that flavonoids possessed antioxidant, antineoplastic and cytotoxic activities. The main objective of this study was to test dichloromethane fraction of resinous exudate of Heliotropium subulatum for their antioxidant, antineoplastic and cytotoxic activities, as well as to search new antioxidant and antineoplastic agents for pharmaceutical formulations. Five flavonoids were isolated from resinous exudate of this plant species and screened for their in vitro and in vivo antioxidant models (DPPH radical scavenging, reducing power, superoxide anion scavenging, metal chelating scavenging systems, catalase and lipid peroxidation), antineoplastic (Sarcoma 180), and cytotoxic (Chinese hamster V79 cells) activities. Tricetin demonstrated maximum antioxidant activity against both in vitro and in vivo experimental systems while galangin exhibited maximum inhibition (78.35%) at a dose of 10 lg/kg/day against Sarcoma 180. Similarly, it was found that galangin also showed highest activity (21.1 ± 0.15%) at a concentration of 70 lg/ml to Chinese hamster V79 cells. The observed results suggest that tricetin has a potential to scavenge free radicals in both in vitro and in vivo models while the galangin could be considered as antitumor and cytotoxic agent.

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Section: Discussionsupporting

confidence: 93%

Flavonoids from Heliotropium subulatum exudate and their evaluation for antioxidant, antineoplastic and cytotoxic activities II

2016

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“…Other studies also reported galangin’s ability to suppress cell proliferation and induce apoptosis in several other cancer cell lines [2,7,8]. These observations strongly suggest that galangin is a potential antitumor agent.…”

Section: Discussionsupporting

confidence: 52%

Galangin Induces Autophagy through Upregulation of p53 in HepG2 Cells

Wen

Wu²,

Luo³

et al. 2012

Pharmacology

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Aim: To investigate the mechanism by which galangin, a polyphenolic compound derived from medicinal herbs, induces autophagy of HepG2 cells. Methods: The MTT [3-(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl-tetrazolium bromide] assay was used to measure cell viability. Apoptosis was evaluated by TUNEL assay with flow cytometry, and PARP cleavage was detected by Western blotting. Autophagy was measured by fluorescence microscopy and transmission electron microscopy. Protein expressions were detected by Western blotting. Pifithrin-α was used for pretreatment and siRNA was used to knock down p53 expression to explore the pathway mediated by galangin in HepG2 cells. Furthermore, Hep3B cells were used to express the exogenous wild-type p53. Results: Galangin treatment inhibited cell proliferation and induced autophagy (130 µmol/l) and apoptosis (370 µmol/l). In particular, galangin treatment in HepG2 cells caused (1) an accumulation of autophagosomes, (2) elevated levels of microtubule-associated protein light chain 3, and (3) an increased percentage of cells with vacuoles. p53 expression was also increased. The galangin-induced autophagy was attenuated by the inhibition of p53 in HepG2 cells, and overexpression of p53 in Hep3B cells restored the galangin-induced higher percentage of cells with vacuoles to normal level. Conclusion: Our results indicate that galangin not only induced apoptosis but also prompted cell autophagy in different concentrations. Galangin mediates autophagy through a p53-dependent pathway in HepG2 cells. Our findings may help in the discovery of a chemotherapeutic drug with the novel pattern of inhibiting cell proliferation for the treatment of hepatocellular carcinoma cells.

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“…A large variety of chemotherapeutic agents induce apoptosis in susceptible cell lines [19][20][21][22]. The cell line studied here, K562, is an erythroleukemia cell line; immunoblotting and various activity assays showed that caspase 3, an enzyme that cleaves full length poly (ADP-ribose) polymerase (PARP), is activated in several human leukemia lines treated with apoptosis inducing agents [23].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of uridine-cytidine kinase like-1 decreases proliferation and enhances tumor susceptibility to lysis by apoptotic agents and natural killer cells

Ambrose

Kornbluth

2009

Apoptosis

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Natural killer (NK) cells target and kill tumor cells by direct anti-tumor cytotoxicity. NK lytic-associated molecule (NKLAM) is a protein involved in this cytolytic function. Acting as an E3 ubiquitin ligase, NKLAM binds to and ubiquitinates a novel protein, uridine-cytidine kinase like-1 (UCKL-1), targeting it for degradation. However, UCKL-1's function in tumor cell survival and NK cell cytotoxicity is unknown. UCKL-1's homology to uridine kinases and over expression in tumor cells suggests a role for UCKL-1 in tumor growth and/or survival. We propose that NKLAM and UCKL-1 interact in the tumor cell, where degradation of UCKL-1 leads to increased tumor cell apoptosis. Here we use RNA interference to downregulate UCKL-1 expression in K562 erythroleukemia cells. It was seen that downregulation of UCKL-1 initiated apoptosis and slowed the cell cycle, resulting in lower growth in the small interfering UCKL-1 RNA treated K562 cell culture. In addition, the chemotherapeutic agent staurosporine was seen to be more effective in inducing cell death by apoptosis in UCKL-1 depleted K562 cells compared with controls. We also found that UCKL-1 depleted K562 cells were more susceptible to NK mediated cytolysis than controls. These results indicate a role for UCKL-1 in tumor cell survival and suggest possible therapeutic potential of UCKL-1 inhibitors in cancer treatment.

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Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

Cited by 68 publications

References 26 publications

Flavonoids from Heliotropium subulatum exudate and their evaluation for antioxidant, antineoplastic and cytotoxic activities II

Flavonoids from Heliotropium subulatum exudate and their evaluation for antioxidant, antineoplastic and cytotoxic activities II

Galangin Induces Autophagy through Upregulation of p53 in HepG2 Cells

Downregulation of uridine-cytidine kinase like-1 decreases proliferation and enhances tumor susceptibility to lysis by apoptotic agents and natural killer cells

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