Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells

Kang, Kyoung Ah; Piao, Mei Jing; Ryu, Yea Seong; Hyun, Yu Jae; Park, Jeong Eon; Shilnikova, Kristina; Zhen, Ao Xuan; Kang, Hee Kyoung; Koh, Young Sang; Jeong, Young Jin; Hyun, Jin Won

doi:10.3892/ijo.2017.4091

Cited by 128 publications

(89 citation statements)

References 48 publications

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“…Luteolin is a flavonoid that has been indicated to arrest the cell cycle and induce apoptosis in a variety of different cancer types (13,14,27). In the present study, the results of the MTT assay demonstrated that luteolin exhibited cytotoxicity on HT29 cell in a concentration-and time-dependent manner, which is consistent with the results of other studies (17,30).…”

Section: Discussionsupporting

confidence: 93%

Luteolin induces mitochondrial apoptosis in HT29 cells by inhibiting the Nrf2/ARE signaling pathway

et al. 2020

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The aim of the current study was to investigate luteolin-induced apoptosis and the molecular mechanisms underlying it in HT29 cells. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to assess the cytotoxicity of luteolin on HT29 cells, and a dichloro-dihydro-fluorescein diacetate assay was used to measure cellular levels of reactive oxygen species (ROS). The effects of luteolin on the mitochondrial membrane potential were also evaluated. Bax and Bcl-2 mRNA expression were determined using reverse transcription-quantitative PCR. Additionally, western blot analysis was performed to assess changes in cytochrome c and caspase-3 protein expression. Localization of nuclear factor erythroid 2-related factor 2 (Nrf2) in the nucleus was also assessed using immunofluorescence. Luteolin exhibited cytotoxicity on HT29 cells in a time-and concentration-dependent manner. Additionally, ROS production was indicated to be increased and ROS scavenging was decreased, which resulted in a significant increase in the levels of ROS in the cells. The mitochondrial membrane potential was indicated to decrease following luteolin treatment. At the molecular level, luteolin significantly increased the mRNA expression of Bax and the protein expression of cytochrome c, caspase-3, p47 phox and p22 phox . The results revealed that luteolin decreased Bcl-2 protein expression and inhibited the nuclear localization of Nrf2. In conclusion, the current study indicated that luteolin inhibited HT29 cell proliferation and induced apoptosis via the mitochondrial pathway.

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Section: Discussionsupporting

confidence: 93%

Luteolin induces mitochondrial apoptosis in HT29 cells by inhibiting the Nrf2/ARE signaling pathway

et al. 2020

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“…CMAC is a GSH‐sensitive dye and commonly used to measure intracellular GSH levels correlated with glutathione peroxidase (GPx) activity (Kang et al, 2017). Blue CMAC staining showed a lower blue fluorescence intensity of GPx activity in cells treated with 0.5 mM ASA compared with the other groups, showing inactivation of the antioxidant system ( p < .05; Figure 4a,b).…”

Section: Resultsmentioning

confidence: 99%

Arachidonic acid alleviates the detrimental effects of acetylsalicylic acid on human granulosa cells performance in vitro

Khajeh

Nouri

Ghasemzadeh

et al. 2020

Molecular Reproduction Devel

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Here, we investigated the biological effects of arachidonic acid (AA) in human cumulus granulosa cells (CGCs) after exposure to ASA. Cells were isolated from the follicular fluid and incubated with 0.5 mM acetylsalicylic acid (ASA) and 50 µM AA.Cell viability was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. E 2 and P 4 levels were measured by chemiluminescence assay.Expression of genes including CYP19A1, FACN, and SCD1 was measured by real-time polymerase chain reaction assay. Oxidative status was analyzed by monitoring glutathione peroxidase activity. The fatty acid profile was analyzed by the gas chromatography technique. Enzyme-linked immunosorbent assay was used to measure prostaglandin E 2 (PGE 2 ) in CGCs after exposure to ASA and AA. Protein levels of the estrogen receptor were studied by immunofluorescence staining. Ultrastructural changes were evaluated by transmission electron microscopy imaging.ASA treatment reduced E 2 production, Cyp19a1 expression, glutathione peroxidase (GPx) activity, and estradiol receptor expression in CGCs. The addition of AA prevented the ASA-induced E 2 reduction (p < .05) and expression of Cyp19a1.Moreover, AA increased the antioxidant capacity of CGCs exposed to ASA by promoting GPx activity (p < .05). AA increased monounsaturated fatty acid/ saturated fatty acid ratio compared with the ASA group (p < .05). AA supplementation triggered the synthesis and secretion of PGE 2 in ASA-treated CGCS (p < .05). Cytoplasmic vacuolation observed in the ASA group and treatment with AA intensified vacuolation rate. The expression of the estrogen receptor was increased

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“…Detailed procedure was described elsewhere [13]. The antibodies against GTPBP4 (ab92342), TNFRSF10B (ab199357), MDM2 (ab16895), p53, CCND1 (ab134175), FAS (ab82419), PTEN (ab79156), CDKN1A (ab109520) and GAPDH (ab9485) were purchased from Abcam.…”

Section: Methodsmentioning

confidence: 99%

GTPBP4 Promotes Gastric Cancer Progression via Regulating P53 Activity

Pang

Zhu

et al. 2018

Cell Physiol Biochem

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Background/Aims: gastric cancer is a serious health concern with high morbidity and mortality. Therefore, it is urgent to find novel targets for gastric cancer diagnosis and treatment. Methods: qRT-PCR and immunohistochemistry assays were used to detect GTPBP4 expression in gastric cancer tissues, and gastric cancer and gastric epithelial cells. Lentivirus infection was used to construct GTPBP4 stable knockdown cells. Annexin V/PI apoptosis, CCK8, EdU incorporation and cell clone formation analysis were performed to evaluate the effects of GTPBP4 on gastric cancer cell proliferation and apoptosis. Further RNA-based high-throughput sequencing and co-IP assays were constructed to explore the related mechanisms contributing to GTPBP4-mediated effects. Results: GTPBP4 expression was significantly increased in gastric cancer tissues compared with that in adjacent normal tissues, and positively correlated with gastric cancer stages. Meanwhile, GTPBP4 level was markedly upregulated in gastric cancer cells than in gastric epithelial cells. Additionaly, stable knockdown of GTPBP4 inhibited cell proliferation and promoted cell apoptosis. Mechanistically, p53 and its related signaling were significantly activated in GTPBP4 stable knockdown cells. And GTPBP4 interacted with p53 in gastric cancer cells. Conclusions: our results provide insights into mechanistic regulation and linkage of the GTPBP4-p53 in gastric cancer, and also a valuable potential target for gastric cancer.

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Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells

Cited by 128 publications

References 48 publications

Luteolin induces mitochondrial apoptosis in HT29 cells by inhibiting the Nrf2/ARE signaling pathway

Luteolin induces mitochondrial apoptosis in HT29 cells by inhibiting the Nrf2/ARE signaling pathway

Arachidonic acid alleviates the detrimental effects of acetylsalicylic acid on human granulosa cells performance in vitro

GTPBP4 Promotes Gastric Cancer Progression via Regulating P53 Activity

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