Arsenite induces cell transformation by reactive oxygen species, AKT, ERK1/2, and p70S6K1

Carpenter, Richard L.; Jiang, Yue; Yi, Jing; He, Jiang; Rojanasakul, Yon; Liu, Lingzhi; Jiang, Bing‐Hua

doi:10.1016/j.bbrc.2011.09.102

Cited by 63 publications

(55 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In concordance, the work of Schwerdtle et al (2003) described that trivalent arsenicals were able to induce ODD in cultured human cells at pathologically relevant concentrations (Schwerdtle et al 2003). Back to the case of inorganic arsenic, recent works described that exposure of lung epithelial cells to arsenite retrieved increased proliferation rates and gain of anchorage-independent cell growth that were reverted by inhibiting ROS production with catalase (Carpenter et al 2011). In the same lung target cells, other authors showed that ROS modulate arsenic-induced tumor growth and angiogenesis by downregulating several miRNAs in control of such transformation features (He et al 2014).…”

Section: Discussionmentioning

confidence: 87%

Oxidative DNA damage enhances the carcinogenic potential of in vitro chronic arsenic exposures

et al. 2015

View full text Add to dashboard Cite

Chronic exposure to arsenic is known to increase the incidence of cancer in humans. Our previous work demonstrated that environmentally relevant arsenic exposures generate an accelerated accumulation of pre-carcinogen 8-OH-dG DNA lesions under Ogg1-deficient backgrounds, but it remains unproved whether this observed arsenic-induced oxidative DNA damage (ODD) is certainly important in terms of cancer. Here, isogenic MEF Ogg1 (+/+) cells and MEF Ogg1 (-/-) cells-unable to properly eliminate 8-OH-dG from DNA-were exposed to 0.5, 1 and 2 µM of sodium arsenite for 40 weeks. The acquisition of an in vitro cancer-like phenotype was assessed throughout the exposure; matrix metalloproteinase (MMP) activities were measured by zymography, colony formation and promotion were evaluated by soft agar assay, and cellular invasiveness was measured by the transwell assay. Alterations in cellular morphology, growth and differentiation status were also included as complementary measures of transformation. MEF Ogg1 (-/-) cells showed a cancer-associated phenotype after 30 weeks of exposure, as indicated by morphological changes, increased proliferation, deregulated differentiation status, increased MMPs secretion, anchorage-independent cell growth and enhancement of tumor growth and invasiveness. Conversely, MEF Ogg1 (+/+) cells did not present changes in morphology or proliferation, exhibited a milder degree of gene deregulation and needed 10 weeks of additional exposure to the highest arsenite doses to show tumor enhancing effects. Thus, Ogg1 genetic background and arsenic-induced 8-OH-dG proved relevant for arsenic-mediated carcinogenic effects. To our knowledge, this is the first study directly linking ODD with arsenic carcinogenesis.

show abstract

Section: Discussionmentioning

confidence: 87%

Oxidative DNA damage enhances the carcinogenic potential of in vitro chronic arsenic exposures

et al. 2015

View full text Add to dashboard Cite

show abstract

“…p70S6K was shown to be a signaling molecule, which is involved in the regulation of a series of physiological processes in protein synthesis. Once activated, p70S6K1 was shown to promote the reconstruction of actin filaments (20)(21)(22). Therefore, the abnormal activation of the PI3K̸Akt pathway in cancer cells may promote their migration and proliferation.…”

Section: B Cmentioning

confidence: 99%

“…Total RNA was extracted from HT29 cells treated with different concentrations of ABGE (20,50 and 100 mg̸ml, with 0/0.1%DMSO vehicle as the control) for 24 h, using TRIzol reagent (Invitrogen Life Technologies, Carlsbad, CA, USA), according to the manufacturer's instructions, and was quantified by spectrophotometry. The reverse transcription reaction was performed using total RNA.…”

Section: Quantitative Polymerase Chain Reaction (Qpcr)mentioning

confidence: 99%

Aged black garlic extract inhibits HT29 colon cancer cell growth via the PI3K/Akt signaling pathway

Yang

Liu

et al. 2014

Biomedical Reports

View full text Add to dashboard Cite

Abstract. Accumulating evidence indicates that aged black garlic extract (ABGE) may prove beneficial in preventing or inhibiting oncogenesis; however, the underlying mechanisms have not been fully elucidated. The present study aimed to investigate the effects of ABGE on the proliferation and apoptosis of HT29 colon cancer cells. Our results demonstrated that ABGE inhibited HT29 cell growth via the induction of apoptosis and cell cycle arrest. We further investigated the phosphatidylinositol 3-kinase̸protein kinase B (PI3K̸Akt) signal transduction pathway and the molecular mechanisms underlying the ABGE-induced inhibition of HT29 cell proliferation. We observed that ABGE may regulate the function of the PI3K̸Akt pathway through upregulating PTEN and downregulating Akt and p-Akt expression, as well as suppressing its downstream target, 70-kDa ribosomal protein S6 kinase 1, at the mRNA and protein levels. In conclusion, these findings suggest that the PI3K̸Akt signal transduction pathway is crucial for the development of colon cancer. ABGE inhibited the growth and induced apoptosis in HT29 cells through the inhibition of the PI3K̸Akt pathway, suggesting that ABGE may be effective in the prevention and treatment of colon cancer in humans.

show abstract

“…To study whether nanoparticles of WC-Co can stimulate ROS generation, BEAS-2B cells were seeded on the coverslips, and cultured overnight, then treated with solvent, fine particles, or nano particles. The production of ROS was detected by DCFH-DA staining as previously described [23,24]. The nano-sized WC-Co at 5 μg/cm 2 induced high levels of ROS production in the cells, while the treatment of cells with the solvent or the fine size WC-Co at 5 μg/cm 2 did not increase ROS generation (Fig.…”

Section: Wc-co Nanoparticles Induced Reactive Oxygen Species (Ros) Prmentioning

confidence: 99%

Tungsten Carbide-Cobalt Nanoparticles Induce Reactive Oxygen Species, AKT, ERK, AP-1, NF-κB, VEGF, and Angiogenesis

Liu

Ding

Zheng

et al. 2015

Biol Trace Elem Res

Self Cite

View full text Add to dashboard Cite

Powder mixtures of tungsten carbide and metallic cobalt (WC-Co) are widely used in various products. Nanoparticles are engineered structures with at least one dimension of 100 nm or smaller. WC-Co is known to be associated with lung injury and diseases. Angiogenesis is a key process during vasculature, carcinogenesis, recovery of injury, and inflammatory diseases. However, the cellular effects of WC-Co nanoparticles on angiogenesis remain to be elucidated. In this study, we investigated angiogenic response and relative mechanisms after exposure to WC-Co nanoparticles. Our results showed that WC-Co nanoparticles at 5 μg/cm(2) induced ROS production which activated AKT and ERK1/2 signaling pathways in lung epithelial cells by reactive oxygen species (ROS) staining and immunoblotting; WC-Co treatment also increased transcriptional activation of AP-1, NF-κB, and VEGF by reporter assay. Further studies demonstrated that ROS are upstream molecules of AKT and ERK signaling pathways; the activation of AP-1, NF-κB, and VEGF was through ROS generation, AKT and ERK1/2 activation. In addition, WC-Co nanoparticles affected the cells to induce angiogenesis by chicken chorioallantoic membrane (CAM) assay. These results illustrate that exposure to WC-Co nanoparticles induces angiogenic response by activating ROS, AKT, and ERK1/2 signaling pathways and the downstream molecules and elucidate the potential molecular mechanisms during this process. This information may be useful for preventing potential damage from nanoparticle exposure in the future.

show abstract

Arsenite induces cell transformation by reactive oxygen species, AKT, ERK1/2, and p70S6K1

Cited by 63 publications

References 33 publications

Oxidative DNA damage enhances the carcinogenic potential of in vitro chronic arsenic exposures

Oxidative DNA damage enhances the carcinogenic potential of in vitro chronic arsenic exposures

Aged black garlic extract inhibits HT29 colon cancer cell growth via the PI3K/Akt signaling pathway

Tungsten Carbide-Cobalt Nanoparticles Induce Reactive Oxygen Species, AKT, ERK, AP-1, NF-κB, VEGF, and Angiogenesis

Contact Info

Product

Resources

About