Curcumin inhibits UV irradiation‐induced oxidative stress and apoptotic biochemical changes in human epidermoid carcinoma A431 cells

Chan, Wen‐Hsiung; Wu, Chih‐Ching; Yu, Jau‐Song

doi:10.1002/jcb.10638

Cited by 140 publications

(112 citation statements)

References 66 publications

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“…Mitochondrial cytochrome c release from CTN-treated cells was assayed as described previously [23]. Caspase 3 activity was measured using the Z-DEVD-AFC fluorogenic substrate [23,24].…”

Section: Cytochrome C Release and Caspase Activity Assaysmentioning

confidence: 99%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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The mycotoxin CTN (citrinin), a natural contaminant in foodstuffs and animal feeds, has cytotoxic and genotoxic effects on various mammalian cells. CTN is known to cause cell injury, including apoptosis, but the precise regulatory mechanisms of CTN action, particularly in stem cells and embryos, are currently unclear. In the present paper, I report that CTN has cytotoxic effects on mouse embryonic stem cells and blastocysts, and is associated with defects in their subsequent development, both in vitro and in vivo. Experiments in embryonic stem cells (ESC-B5) showed that CTN induces apoptosis via ROS (reactive oxygen species) generation, increased Bax/Bcl-2 ratio, loss of MMP (mitochondrial membrane potential), induction of cytochrome c release, and activation of caspase 3. In this model, CTN triggers cell death via inactivation of the HSP90 [a 90 kDa isoform of the HSP (heat-shock protein) family proteins]/multichaperone complex and subsequent degradation of Ras and Raf-1, further inhibiting anti-apoptotic processes, such as the Ras → ERK (extracellular-signal-regulated kinase) signal transduction pathway. In addition, CTN causes early developmental injury in mouse ESCs and blastocysts in vitro. Lastly, using an in vivo mouse model, I show that consumption of drinking water containing 10 µM CTN results in blastocyst apoptosis and early embryonic developmental injury. Collectively, these findings show for the first time that CTN induces ROS and mitochondria-dependent apoptotic processes, inhibits Ras → ERK survival signalling via inactivation of the HSP90/multichaperone complex, and causes developmental injury in vivo.

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“…Mitochondrial cytochrome c release from CTN-treated cells was assayed as described previously [23]. Caspase 3 activity was measured using the Z-DEVD-AFC fluorogenic substrate [23,24].…”

Section: Cytochrome C Release and Caspase Activity Assaysmentioning

confidence: 99%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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“…9 Several studies have provided evidence that intracellular production of reactive oxygen species can lead directly to activation of mitochondrial permeability transition, loss of mitochondrial membrane potential, and cytochrome c release from mitochondria into the cytoplasm, followed by activation of the caspase cascade, and, ultimately, apoptotic cell death. 10 Further, according to the recent literature, various physicochemical properties of nanoparticles contribute to the cytotoxic mechanisms of nanoparticles. Because commonly used chemicals in aqueous media are unchanged during the exposure time and their intrinsic properties are well understood, treatment conditions, such as concentration and exposure time, provide sufficient information to produce reproducible and reliable dose-response relationships for the corresponding compound.…”

Section: Introductionmentioning

confidence: 99%

Titanium dioxide induces apoptotic cell death through reactive oxygen species-mediated Fas upregulation and Bax activation

Yoo¹,

Yoon²,

Kwon³

et al. 2012

IJN

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Background: Titanium dioxide (TiO 2 ) has been widely used in many areas, including biomedicine, cosmetics, and environmental engineering. Recently, it has become evident that some TiO 2 particles have a considerable cytotoxic effect in normal human cells. However, the molecular basis for the cytotoxicity of TiO 2 has yet to be defined. Methods and results:In this study, we demonstrated that combined treatment with TiO 2 nanoparticles sized less than 100 nm and ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species-dependent upregulation of Fas and conformational activation of Bax in normal human cells. Treatment with P25 TiO 2 nanoparticles with a hydrodynamic size distribution centered around 70 nm ) together with ultraviolet A irradiation-induced caspase-dependent apoptotic cell death, accompanied by transcriptional upregulation of the death receptor, Fas, and conformational activation of Bax. In line with these results, knockdown of either Fas or Bax with specific siRNA significantly inhibited TiO 2 -induced apoptotic cell death. Moreover, inhibition of reactive oxygen species with an antioxidant, N-acetyl-L-cysteine, clearly suppressed upregulation of Fas, conformational activation of Bax, and subsequent apoptotic cell death in response to combination treatment using TiO 2 P25-70 and ultraviolet A irradiation. Conclusion:These results indicate that sub-100 nm sized TiO 2 treatment under ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species-mediated upregulation of the death receptor, Fas, and activation of the preapoptotic protein, Bax. Elucidating the molecular mechanisms by which nanosized particles induce activation of cell death signaling pathways would be critical for the development of prevention strategies to minimize the cytotoxicity of nanomaterials.

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“…Curcumin is shown to affect the phosphorylation of MAPK1/3 and also reported to regulate the cleavage and activation of p21 (RAC1)-activated kinase 2 (PAK2). 10,[24][25][26] In addition, curcumin has also been reported to affect the autophosphorylation of epidermal growth factor receptor (EGFR) where it has also been shown to decrease phosphorylation of EGFR. 27,28 Our group has studied dysregulation in tyrosine kinases in the same cell line, Cal 27, in response to curcumin.…”

Section: Discussionmentioning

confidence: 99%

Investigation of curcumin-mediated signalling pathways in head and neck squamous cell carcinoma

Nanjappa

Sathe

Jain

et al. 2017

Translational Research in Oral Oncology

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Objectives: Curcumin has been shown to exhibit anti-neoplastic effects. However, due to its poor bioavailability, the use of curcumin as an anti-cancer drug is limited. Thus, it is necessary to identify molecules as an alternative to curcumin that could serve as anti-cancer targets. In this study, we attempted to understand the underlying curcumin-mediated signalling pathways contributing to anti-neoplastic effects of curcumin. Methods: We carried out mass spectrometry-based phosphoproteomic analysis of head and neck cancer cell line, CAL 27, treated with and without curcumin to identify curcumin-mediated signalling pathways. Serine/threonine kinases were enriched using titanium dioxide.Results: This resulted in the identification of 5921 phosphopeptides corresponding to 1878 proteins. Of these, 275 and 183 phosphopeptides corresponding to 335 and 242 proteins (!2.0-fold) were found to be hyper-and hypo-phosphorylated, respectively, in response to curcumin treatment. Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2), a serine/ threonine kinase, and its downstream target protein kinase AMP-activated non-catalytic subunit beta 1 (PRKAB1) were found to be hypo-phosphorylated when treated with curcumin. Further, silencing or inhibiting CaMKK2 resulted in decreased invasion and colony forming ability of not only CAL 27 cells but also other head and neck squamous cell carcinoma (HNSCC) cell lines. Further, Western blot analysis showed that curcumin-mediated signalling is corroborated by CaMKK2. Conclusions: Taken together, our results suggest that CaMKK2 could be a novel therapeutic target in HNSCC and can serve as an alternative to curcumin.

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Curcumin inhibits UV irradiation‐induced oxidative stress and apoptotic biochemical changes in human epidermoid carcinoma A431 cells

Cited by 140 publications

References 66 publications

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Titanium dioxide induces apoptotic cell death through reactive oxygen species-mediated Fas upregulation and Bax activation

Investigation of curcumin-mediated signalling pathways in head and neck squamous cell carcinoma

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