Studies showing arsenic inhibiting PI3K/AKT/mTOR pathway

Arsenic CompoundTreatmentCell TypeTechnique PlatformPathway EffectTissue TypeReference
NaAsO20–2 μM for 7 days3T3-L1qRT-PCR, Western blotting, immunofluorescence,Inactivation of AKTAdipocytesXue et al. (2011)
As2O30–10 μM for 48 h or 5 μM for up to 72 hSW1353MTT, Western blotting, cell viability, clone formation, apoptosis, immunofluorescence,Inactivation of AKT and mTORChondrosarcomaJiao et al. (2015)
As4O61 μM for 48 hSW620Cell viability, ROS generation, cell cycle, nuclear staining, Western blotting, inhibitors assayDecreased PI3K/AKTColorectal cancerNagappan et al. (2017)
As2O30–16 μM for 24 hSGC-7901Cell viability, mitochondrial membrane potential, apoptosis, Western blottingInactivation of AKTGastric cancerGao et al. (2014)
As2O33 mg/kg for 7 daysMale Wistar ratsHistologic analysis, Western blottingInactivation of PI3K and AKTLiverZhang et al. (2017)
NANAU937NAInactivation of AKTMyeloid cancerChoi et al. (2002)
As2O31 μM for NB4 and 4 μM for THP1 cells for 4 hNNA, B4, THP1Flow cytometry, cell proliferation, viability, apoptosis, necrosis, ROS and GSH level, immunoblottingATO alone has no effect on AKT, only with 2-DG (2-deoxy-d-glucose)Myeloid cancerEstañ et al. (2012)
As2O31 μM for 24 h in NB4 cells and 10 μM for 16 h in MGC803 cellsNB4 and MGC803Cell viability, cell cycle, Western blottingInactivation of PI3K and AKTGastric and myeloid cancerLi et al. (2009)
As2S23.02–13.06 μM for 24 or 48 h treatment143B, MG-63, U-2OS, and HOSCell viability, clone formation, cell cycle, apoptosis, histopathology, immunohistochemistry, human osteosarcoma xenograft, Western blotting, ROS generationInactivation of AKT and mTOROsteosarcomaWang et al. (2017)
As2O33 μM for 48 hB-CLLCell apoptosis, ROS, Western blottingInactivation of PI3K and AKTPeripheral bloodRedondo-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.