Expression of the thioredoxin system in an in vivo-like cancer cell environment upon auranofin treatment

Selenoproteins in Tumorigenesis and Cancer Progression

“…In these experiments, cells with loss of TrxR1 were much less efficient at forming tumor and metastasis in vivo, and tumors that did form still expressed TrxR1 due to loss of the targeting construct. In breast cancer cells, TrxR1 appears to mediate the epithelial-to-mesenchymal transition (EMT), as loss of TrxR1 pushes cells towards an epithelial phenotype while overexpression enhanced invasion in Boyden chamber assays (Bhatia et al, 2016;Dong et al, 2016). Together, these results offer strong evidence that TrxR's primarily function is that of an oncogene in malignant cells.…”

Thioredoxin Confers Intrinsic Resistance to Cytostatic Drugs in Human Glioma Cells

“…In invasive cervical carcinomas, Trx upregulation was detected in tumor microregions suffering from hypoxia, suggesting hypoxia-inducible factor-1 α (HIF-1α) induction, which is entailed by PI3K/AKT pathway activation [ 33 ]. Consistently, hypoxia was also linked to increased Trx levels and sensitivity to TrxR inhibition in cancer cells cultured in monolayers and 3D spheroid-based culture models [ 34 ]. Additionally, TRX gene transfection of lymphoid and breast cancer cells or Trx protein supplemented to tissue culture medium has been reported to prevent apoptosis and increase cell invasion [ 11 , 17 ].…”

The Role of Biomimetic Hypoxia on Cancer Cell Behaviour in 3D Models: A Systematic Review

“…HIF1's activation has been shown to upregulate EMT within 18hrs of exposure to 1% oxygen and upregulation of angiogenesis related markers can be seen within 2 to 4 h [126]. One study we encountered explored cycling hypoxia and reoxygenation in their tumour cultures [61]. Although evidence does show acute hypoxia exposure is sufficient in tumorigenesis, the repeated cycles of hypoxia/reoxygenation have also been linked with increased angiogenesis, and genetic instability due to induction of DNA damage and impaired DNA repair mechanisms [127].…”

“…We identified a total of 42 publications [16,19,22,23,30,41,42,45,49,52,56,59,61,64,68,72,74,80,85,89,[100][101][102][103]105,106,[108][109][110][111][112][113][114][115][116][117][118][119][120][121][122][123] comparing cell response to chemotherapy and other interventions between 2D and 3D in vitro tumour models, using a variety of anticancer agents and taking into account any publications which involved more than one type of anticancer agents, yielding in total 85 separate findings, including 79 outcomes concerning chemotherapy agents, three involving radiotherapy, and a further five exploring natural compound agents such as orange-peel flavones. The definitions for drug response varied throughout the studies in terms of markers used and duration over which drug responses were measured.…”