Generation of reactive oxygen species mediates butein-induced apoptosis in neuroblastoma cells

Chen, Yahui; Yeh, Chi-Wei; Lo, Hui‐Chen; Su, Shih‐Li; Hseu, You‐Cheng; Hsu, Li‐Sung

doi:10.3892/or.2012.1632

Cited by 44 publications

(28 citation statements)

References 23 publications

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“…The A549 cells were seeded in 24-well plates at a density of 2x10 4 /ml and were treated with 0, 25, 50, 100, 200 and 300 µM naringenin for 24 and 48 h. Following the treatment, the cells were incubated with fresh medium containing 5.0 g/l MTT, and incubated at 37˚C for an additional 2 h. After washing with PBS, the sediments were dissolved in 1 ml isopropanol and the absorbance at 563 nm was determined. The relative viability rate was determined based on the absorbance at 563 nm of each sediment compared with vehicle-treated groups.…”

Section: Methodsmentioning

confidence: 99%

“…For example, butein inhibits the migration and invasion of bladder cancer cells by reducing the expression of extracellular signal-regulated kinase 1/2 and its activities (3). In addition, butein has been found to elevate reactive oxygen species (ROS) levels and trigger apoptosis in neuroblastoma (4) and breast cancer cells (5,6). Moreover, shikonin induces apoptosis in osteosarcoma cells via the generation of ROS (7).…”

Section: Introductionmentioning

confidence: 99%

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Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Chang

Lai

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Lung cancer is among the most common causes of cancer-related mortality. It has a high mortality rate and resistance to chemotherapy due to its high metastatic potential. Naringenin, a bioactive compound identified in several fruits, displays anti-inflammatory and antitumor effects. Furthermore, naringenin mitigates the migration of several human cancer cell types. However, the effects of naringenin on lung cancer remain unclear. The current study investigated the mechanisms of naringenin on the migration of lung cancer A549 cells. The results indicate that significant alteration in A549 cell proliferation was observed in response to naringenin (0-300 µM) treatment for 24 and 48 h. Furthermore, a dose-dependent migration inhibition of A549 in the presence of naringenin was observed by healing and transwell migration assays. In addition, a zymography assay revealed that naringenin exhibited a concentration-dependent inhibition of matrix metalloproteinase (MMP)-2 and -9 activities. Furthermore, naringenin also inhibited the activities of AKT in a dose-dependent manner. These observations indicated that naringenin inhibited the migration of lung cancer A549 cells through several mechanisms, including the inhibition of AKT activities and reduction of MMP-2 and -9 activities.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Chang

Lai

et al. 2016

Experimental and Therapeutic Medicine

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“…Butein has been shown to increase ROS levels in neuroblastoma cells and breast cancer cells [31,36] and also functions as antioxidant for liver stellate cells and keratinocytes [21,37]. OA chondrocytes treated with Butein showed no increase in ROS levels as measured by DCFDA (Fig.…”

Section: Butein Activated Autophagy Via Ampk/tsc2/ulk1/mtor Pathway Imentioning

confidence: 99%

“…There are reports that have shown that Butein reduces cell viability and enhances apoptosis in multiple cancer cells including ovarian cancer cells [30] cervical cancer cells [23], neuroblastoma [31] and T-cell lymphoma [32]. In order to study the effects of Butein on the viability of OA chondrocytes, OA chondrocytes were treated with different concentrations of Butein [0.6 μg/ml -10 μg/ml (or 2.25 μM -36 μM)] for 24 hr or with 10 μg/ml Butein for up to 72 hr and the viability was analyzed by MTT assay.…”

Section: Butein Did Not Affect the Viability Of Oa Chondrocytes In Vitromentioning

confidence: 99%

Butein Activates Autophagy Through AMPK/TSC2/ULK1/mTOR Pathway to Inhibit IL-6 Expression in IL-1β Stimulated Human Chondrocytes

Ansari

Ahmad

Haqqi

2018

Cell Physiol Biochem

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Background/Aims: Butein (2’,3,4,4’-Tetrahydroxychalcone), a polyphenol produced by several plants including Butea monoserpma, has been reported to exert potent anti-inflammatory activity but the mechanism remains unknown. In the present work we investigated the mechanism of Butein-mediated suppression of IL-6 expression in normal and human osteoarthritis (OA) chondrocytes under pathological conditions. Methods: Expression level of interleukin-6 (IL-6) protein in OA cartilage was analyzed by immunohistochemistry using a validated antibody. Chondrocytes derived from normal or OA cartilage by enzymatic digestion were pretreated with Butein followed by stimulation with interleukin-1β (IL-1β) and the levels of IL-6 mRNA were quantified by TaqMan assay and the protein levels were measured by Western immunoblotting. Autophagy activation was determined by Western blotting and confocal microscopy. Autophagy was inhibited by siRNA mediated knockdown of ATG5. Results: Expression of IL-6 protein was high in the OA cartilage compared to smooth cartilage from the same patient. OA chondrocytes and cartilage explants stimulated with IL-1β showed high level expression of IL-6 mRNA and protein. Butein increased the phosphorylation of AMPKα^Thr-172, TSC2^Ser-1387 and ULK1^Ser-317 and inhibited the phosphorylation of mTOR^Ser-2448 and its downstream target p70S6K and increased autophagy flux that correlated with the suppression of the IL-1β mediated expression of IL-6 in normal and OA chondrocytes. In OA chondrocytes with siRNA-mediated knockdown of ATG5 expression, treatment with Butein failed to activate autophagy and abrogated the suppression of IL-1β induced IL-6 expression. Conclusion: Our findings demonstrate for the first time that Butein activate autophagy in OA chondrocytes via AMPK/TSC2/ULK1/mTOR pathway. Additionally, activation of autophagy was essential to block the IL-1β-induced expression of IL-6 in OA chondrocytes. These data support further studies to evaluate the use of Butein or compounds derived from it for the management of OA.

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“…Simultaneously it decreases the Bcl-2/Bax ratio. 9 The ultimate result is marked accentuation of intratumoral apoptosis.…”

Section: 1mentioning

confidence: 99%

Butein and its Emerging Anti-Proliferative and Pro-Apoptotic Effects in Systemic Malignancies

Kapoor

2013

Current Eye Research

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Generation of reactive oxygen species mediates butein-induced apoptosis in neuroblastoma cells

Cited by 44 publications

References 23 publications

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Naringenin inhibits migration of lung cancer cells via the inhibition of matrix metalloproteinases-2 and −9

Butein Activates Autophagy Through AMPK/TSC2/ULK1/mTOR Pathway to Inhibit IL-6 Expression in IL-1β Stimulated Human Chondrocytes

Butein and its Emerging Anti-Proliferative and Pro-Apoptotic Effects in Systemic Malignancies

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