Article Figures & Data
Figures
- Fig. 1.
Graphical representation illustrating the role of the PI3K/AKT/mTOR pathway in promoting cellular growth.
Tables
Arsenic Compound Treatment Cell Type Technique Platform Pathway Effect Tissue Type Reference Arsenite (As 3+) 1.25 μM for 72 h JB6 Cl41 Cell proliferation, cell cycle, gene reporter, PI3 kinase assay, Western blotting, cyclin D1 expression assay, Activated PI3K and AKT Epidermis Ouyang et al. (2006) NaAsO2 0,0.25,1, 5 μM for 26 wk BEAS-2B Cell proliferation, soft agar, immunoblotting, ROS detection, Activated AKT and mTOR Lung Carpenter et al. (2011) AsCl3 10 μM 0–16 h BEAS-2B Western blotting, ELISA, cell migration Activated AKT Lung Liu et al. (2011) AsCl3 0–20 μM 6–12 h BEAS-2B Western blotting, RT-PCR, reporter assay, cell proliferation, transformation assay, ELISA Activated AKT Lung Beezhold et al. (2011) AsCl3 0–20 μM of arsenic chloride for up to 20 wk BEAS-2B RT-PCR, qPCR, RNA immunoprecipitation, immunofluorescence Activated AKT Lung Zhang et al. (2006) NaAsO2 2.5 μM for 6 wk HBEC Cell migration, invasion, Western blotting, immunofluorescence Activated AKT Lung Wang et al. (2012) NaAsO2 0–20 μM for 6 h A375 Western blotting, Activated AKT Skin Li et al. (2015) C6AsNH6O6 1.0 µmol/liter Vascular endothelial cells male Wistar rats and C57BL/6 mice MTT, cell proliferation, migration, tube formation, xenograft, immunohistochemical staining, Western blotting Activated PI3K and AKT Thoracic aorta Wang et al. (2016) NaAsO2 0,1,2,4,8,10 μM SV-HUC-1 RT-PCR, Western blotting, ELISA Activated PI3K and AKT Ureter Wang (2013) BEAS-2B, human bronchial epithelial cells; CLL, chronic lymphocytic leukemia; ELISA, enzyme-linked immunosorbent assay; GSH, glutathione; HBEC, human bronchial epithelial cells; qRT-PCR, quantitative reverse transcription-polymerase chain reaction.
Arsenic Compound Treatment Cell Type Technique Platform Pathway Effect Tissue Type Reference NaAsO2 0–2 μM for 7 days 3T3-L1 qRT-PCR, Western blotting, immunofluorescence, Inactivation of AKT Adipocytes Xue et al. (2011) As2O3 0–10 μM for 48 h or 5 μM for up to 72 h SW1353 MTT, Western blotting, cell viability, clone formation, apoptosis, immunofluorescence, Inactivation of AKT and mTOR Chondrosarcoma Jiao et al. (2015) As4O6 1 μM for 48 h SW620 Cell viability, ROS generation, cell cycle, nuclear staining, Western blotting, inhibitors assay Decreased PI3K/AKT Colorectal cancer Nagappan et al. (2017) As2O3 0–16 μM for 24 h SGC-7901 Cell viability, mitochondrial membrane potential, apoptosis, Western blotting Inactivation of AKT Gastric cancer Gao et al. (2014) As2O3 3 mg/kg for 7 days Male Wistar rats Histologic analysis, Western blotting Inactivation of PI3K and AKT Liver Zhang et al. (2017) NA NA U937 NA Inactivation of AKT Myeloid cancer Choi et al. (2002) As2O3 1 μM for NB4 and 4 μM for THP1 cells for 4 h NNA, B4, THP1 Flow cytometry, cell proliferation, viability, apoptosis, necrosis, ROS and GSH level, immunoblotting ATO alone has no effect on AKT, only with 2-DG (2-deoxy-d-glucose) Myeloid cancer Estañ et al. (2012) As2O3 1 μM for 24 h in NB4 cells and 10 μM for 16 h in MGC803 cells NB4 and MGC803 Cell viability, cell cycle, Western blotting Inactivation of PI3K and AKT Gastric and myeloid cancer Li et al. (2009) As2S2 3.02–13.06 μM for 24 or 48 h treatment 143B, MG-63, U-2OS, and HOS Cell viability, clone formation, cell cycle, apoptosis, histopathology, immunohistochemistry, human osteosarcoma xenograft, Western blotting, ROS generation Inactivation of AKT and mTOR Osteosarcoma Wang et al. (2017) As2O3 3 μM for 48 h B-CLL Cell apoptosis, ROS, Western blotting Inactivation of PI3K and AKT Peripheral blood Redondo-Muñoz et al. (2010) ATO, arsenic trioxide; B-CLL, B-cell chronic lymphocytic leukemia; GSH, glutathione; NA, not applicable; qRT-PCR, quantitative reverse transcription-polymerase chain reaction.
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Arsenic Carcinogenesis: PI3K/Akt/mTOR Signaling Pathway
