Luteolin Induces Apoptosis in Oral Squamous Cancer Cells

Yang, Shun‐Fa; Yang, Wei‐En; Chang, Horng-Rong; Chu, Shu‐Chen; Hsieh, Yih‐Shou

doi:10.1177/154405910808700413

Cited by 98 publications

(73 citation statements)

References 28 publications

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“…The anticancer effect of Lu also is associated with inducing apoptosis, which involves redox regulation, DNA damage, and protein kinases in inhibiting the proliferation of cancer cells and suppressing metastasis and angiogenesis. 6,[10][11][12][13][14][15][16][17] Moreover, Lu has cytotoxicity in cancer cells or immortalized cells, but not in normal cells, meaning that it has fewer side effects when used in treating cancer. 8,12,18 Yet Lu has some drawbacks, such as poor water solubility (,2 × 10 −2 µmol/mL), 19 low oral absorption, 20 and bioavailability (30.4% in rats), 21 which limit its clinical application.…”

Section: Introductionmentioning

confidence: 99%

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Qiu¹,

Gao²,

Wang³

et al. 2013

IJN

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Luteolin (Lu) is one of the flavonoids with anticancer activity, but its poor water solubility limits its use clinically. In this work, we used monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) (MPEG-PCL) micelles to encapsulate Lu by a self-assembly method, creating a water-soluble Lu/MPEG-PCL micelle. These micelles had a mean particle size of 38.6 ± 0.6 nm (polydispersity index = 0.16 ± 0.02), encapsulation efficiency of 98.32% ± 1.12%, and drug loading of 3.93% ± 0.25%. Lu/MPEG-PCL micelles could slowly release Lu in vitro. Encapsulation of Lu in MPEG-PCL micelles improved the half-life (t ½ ; 152.25 ± 49.92 versus [vs] 7.16 ± 1.23 minutes, P = 0.007), area under the curve (0-t) (2914.05 ± 445.17 vs 502.65 ± 140.12 mg/L/minute, P = 0.001), area under the curve (0-∞) (2989.03 ± 433.22 vs 503.81 ± 141.41 mg/L/minute, P = 0.001), and peak concentration (92.70 ± 11.61 vs 38.98 ± 7.73 mg/L, P = 0.003) of Lu when the drug was intravenously administered at a dose of 30 mg/kg in rats. Also, Lu/MPEG-PCL micelles maintained the cytotoxicity of Lu on 4T1 breast cancer cells (IC50 = 6.4 ± 2.30 µg/mL) and C-26 colon carcinoma cells (IC50 = 12.62 ± 2.17 µg/mL) in vitro. These data suggested that encapsulation of Lu into MPEG-PCL micelles created an aqueous formulation of Lu with potential anticancer effect.

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Section: Introductionmentioning

confidence: 99%

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Qiu¹,

Gao²,

Wang³

et al. 2013

IJN

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“…[32,33] In the present study, it is postulated that the cytotoxic activity of EEAC is directly related to the presence of flavonoids especially Rutin. Studies have shown that rutin plays a beneficial role in inhibiting the growth of tumor.…”

Section: Selectivity Indexmentioning

confidence: 70%

Phytochemical Analysis and in Vitro Anticancer Study of Ethanolic Extract of Leaves of Amaranthus Cruentus Linn. Against Colon Cancer Cell Line (Hct-116)

Sekar¹

2017

WJPPS

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Objective: The study is aimed at evaluating the anticancer activity of ethanolic extract of leaves of Amaranthus cruentus Linn. against colon cancer cell lines on the basis of its indigenous use and constituents. Method:The ethanolic extract of the leaves of Amaranthus cruentus prepared by using the soxhlet extraction method was subjected to phytochemical analysis to detect the plethora of secondary metabolities present. The total flavonoid content was determined using aluminium chloride colorimeteric method. The in vitro anticancer activity was studied using MTT assay against HCT -116 (Colon cancer cell line).The toxicity study against normal Vero cell line was also done to determine the selectivity of the extract for inhibiting cancer cells. 5-Fluorouracil was used as standard as it is the first choice of drug for the treatment of colon cancer. Results: The ethanolic extract showed presence of variety of secondary metabolites such as flavonoids, alkaloids, phenols, saponins, steroids and proteins. The IC 50 value of EEAC was 138±4.24 µg/ml and that of 5-fluorouracil was 32.14±1.58 µg/ml against HCT-116. This indicates that the EEAC has cytotoxic effects comparable with 5-Fluorouracil. The IC 50 value of EEAC was 1777±78.25µg/ml and that of 5-fluorouracil was 134.4±5.30 µg/ml against Vero cell line. This showed that the plant produce lesser cytotoxic damage to normal cells compared to standard 5 -Fluorouracil.

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“…At the end of the 28 days of treatment, mice were killed, and tumors were removed, measured, and weighted as previously described. 33,37,38 All animal studies were conducted according to institutional guidelines (Affidavit of Approval of Animal Use Protocol) approved by the Institutional Animal Care and Use Committee (IACUC) of China Medical University (Taichung, Taiwan). …”

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confidence: 99%

Gypenosides Suppress Growth of Human Oral Cancer SAS Cells In Vitro and in a Murine Xenograft Model

Chen

Lai

et al. 2011

Integr Cancer Ther

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Purpose. Gypenosides (Gyp) are the major components of Gynostemma pentaphyllum Makino. The authors investigated the effects of Gyp on cell morphology, viability, cell cycle distribution, and induction of apoptosis in human oral cancer SAS cells and the determination of murine SAS xenograft model in vivo. Experimental design. Flow cytometry was used to quantify the percentage of viable cells; cell cycle distribution; sub-G1 phase (apoptosis); caspase-3, -8, and -9 activity; reactive oxygen species (ROS) production, intracellular Ca 2+ determination; and the level of mitochondrial membrane potential (ΔΨ m ). Western blotting was used to examine levels of apoptosis-associated proteins, and confocal laser microscopy was used to examine the translocation of proteins in cells. Results. Gyp induced morphological changes, decreased the percentage of viable cells, caused G0/G1 phase arrest, and triggered apoptotic cell death in SAS cells. Cell cycle arrest induced by Gyp was associated with apoptosis. The production of ROS, increased intracellular Ca 2+ levels, and the depolarization of ΔΨ m were observed. Gyp increased levels of the proapoptotic protein Bax but inhibited the levels of the antiapoptotic proteins Bcl-2 and Bcl-xl. Gyp also stimulated the release of cytochrome c and Endo G. Translocation of GADD153 to the nucleus was stimulated by Gyp. Gyp in vivo attenuated the size and volume of solid tumors in a murine xenograft model of oral cancer. Conclusions. Gyp-induced cell death occurs through caspase-dependent and caspase-independent apoptotic signaling pathways, and the compound reduced tumor size in a xenograft nu/nu mouse model of oral cancer. Materials and Methods Chemicals, Reagents, and Cell CultureGyp was kindly provided by Dr Jung-Chou Chen (Department of Chinese Medicine, China Medical University, Taichung, Taiwan). 25 Dimethyl sulfoxide (DMSO), propidium iodide (PI), potassium phosphates, ribonuclease-A, Triton X-100, Tris-HCl, and trypan blue were obtained from Sigma Chemical Co (St Louis, MO). 2,7-Dichlorodihydrofluorescein diacetate, DiOC 6 , and Fluo-3/AM were obtained from Molecular Probes/Invitrogen Corp (Eugene, OR). Dulbecco's modified Eagle's medium (DMEM), L-glutamine, fetal bovine serum (FBS), penicillin-streptomycin, and trypsin-EDTA were obtained from GIBCO BRL/Invitrogen Corp (Grand Island, NY). The SAS cell line (human oral squamous cell carcinoma) was obtained from Dr Pei-Jung Lu (Graduate Institute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan). Cells were cultured in DMEM containing 10% FBS, 2 mM L-glutamine, 100 U/mL penicillin, and 100 µg/mL streptomycin in 75 cm 2 tissue culture flasks at 37°C under a humidified 5% CO 2 and 95% air atmosphere as we have previously reported. 22 In Vitro StudiesAssessment of cell morphology and viability. Gyp was prepared and dissolved in DMSO. Cells (2 × 10 5 cells/well) were plated in 12-well plates in 2 mL DMEM and incubated at 37°C for 24 hours. Cells were then treated with 0, 60, 90, 120, 150, and 180 µg/mL G...

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Luteolin Induces Apoptosis in Oral Squamous Cancer Cells

Cited by 98 publications

References 28 publications

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Phytochemical Analysis and in Vitro Anticancer Study of Ethanolic Extract of Leaves of Amaranthus Cruentus Linn. Against Colon Cancer Cell Line (Hct-116)

Gypenosides Suppress Growth of Human Oral Cancer SAS Cells In Vitro and in a Murine Xenograft Model

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Luteolin Induces Apoptosis in Oral Squamous Cancer Cells

Cited by 98 publications

References 28 publications

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(&epsilon;-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(&epsilon;-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Phytochemical Analysis and in Vitro Anticancer Study of Ethanolic Extract of Leaves of Amaranthus Cruentus Linn. Against Colon Cancer Cell Line (Hct-116)

Gypenosides Suppress Growth of Human Oral Cancer SAS Cells In Vitro and in a Murine Xenograft Model

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Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(ε-caprolactone) micelles for the solubilization and in vivo delivery of luteolin