Use of an Aqueous Soluble Tetrazolium/Formazan Assay for Cell Growth Assays in Culture

Cory, Ann H.; Owen, Terence C.; Barltrop, J. A.; Cory, Joseph G.

doi:10.3727/095535491820873191

Cited by 1,379 publications

(1,009 citation statements)

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“…16 This was demonstrated in these experiments ( Figure 5). HIV-1 challenge significantly enhanced expression of TAR 25 + A/tat in SupT1 cells transduced with SV(PolyTAR).…”

Section: Figure 1 Maps Of Sv(polytar) and Sv[u6]tar Sv(polytar): Insupporting

confidence: 67%

“…34 Conversion of MTS into the aqueous soluble formazan occurs via dehydrogenase enzymes found in metabolically active cells, and the quantity of formazan produced, as measured by the amount of 490 nm absorbance, is directly proportional to the number of living cells in culture. 16,34 Detection of polyTAR transcript by RT-PCR SupT1 cells were transduced with SV(polyTAR) constructs as described. Control cells were transduced with SV(HBS).…”

Section: Transduction Of Human T Lymphocyte Cell Linesmentioning

confidence: 99%

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SV40-derived vectors provide effective transgene expression and inhibition of HIV-1 using constitutive, conditional,and pol III promoters

et al. 2001

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“…16 This was demonstrated in these experiments ( Figure 5). HIV-1 challenge significantly enhanced expression of TAR 25 + A/tat in SupT1 cells transduced with SV(PolyTAR).…”

Section: Figure 1 Maps Of Sv(polytar) and Sv[u6]tar Sv(polytar): Insupporting

confidence: 67%

Section: Transduction Of Human T Lymphocyte Cell Linesmentioning

confidence: 99%

SV40-derived vectors provide effective transgene expression and inhibition of HIV-1 using constitutive, conditional,and pol III promoters

et al. 2001

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“…78 This assay of cellular proliferation uses 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2 to 4-sulfophenyl)-2H-tetrazolium salt (MTS; Promega, Madison, MI, USA). Upon addition to medium containing viable cells, MTS is reduced to a water-soluble formazan salt.…”

Section: Cell Survival Assay (Mts Assay)mentioning

confidence: 99%

Impaired homeostasis and phenotypic abnormalities in Prdx6−/−mice lens epithelial cells by reactive oxygen species: increased expression and activation of TGFβ

et al. 2005

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PRDX6, a member of the peroxiredoxins (PRDXs) family, is a key player in the removal of reactive oxygen species (ROS). Using targeted inactivation of the Prdx6 gene, we present evidence that the corresponding protein offsets the deleterious effects of ROS on lens epithelial cells (LECs) and regulates gene expression by limiting its levels. PRDX6-depleted LECs displayed phenotypic alterations and elevated a-smooth muscle actin and big-h3 expression (markers for cataractogenesis), indistinguishable from transforming growth factor b (TGFb)-induced changes. Biochemical assays disclosed enhanced levels of ROS, as well as high expression and activation of TGFb1 in Prdx6 À/À LECs. A CAT assay revealed transcriptional repression of lens epithelium-derived growth factor (LEDGF), HSP27, and aB-crystallin promoter activities in these cells. A gel mobility shift assay demonstrated the attenuation of LEDGF binding to heat shock or stress response elements present in these genes. A supply of PRDX6 toPrdx6 À/À LECs reversed these changes. Based on the above data, we propose a rheostat role for PRDX6 in regulating gene expression by controlling the ROS level to maintain cellular homeostasis.

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“…Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium (MTS) dye-reduction assay measuring mitochondrial respiratory function (Cory et al, 1991). Breast cancer cells (1 × 10 3 well -1 ) were plated in 96-well microtitre plates and treated with bisphosphonates at various concentrations and for different periods of time.…”

Section: Mts Assaymentioning

confidence: 99%

Bisphosphonates induce apoptosis in human breast cancer cell lines

et al. 2000

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Over 80% of women with advanced breast cancer ultimately develop bone metastases which account significantly for morbidity and mortality. Breast cancer metastases in bone can cause intractable pain, bone fracture, spinal cord compression and hypercalcaemia. It also signifies that the malignant process is incurable since, once tumour cells become lodged in the skeleton, therapy can only be given with palliative intent. This includes analgesics, radiation therapy and systemic treatments such as hormone or chemotherapy. The events leading to the development of bone lesions in patients with carcinoma of the breast are poorly understood. However, histomorphometric studies have shown that tumour cells are adjacent to actively resorbing osteoclasts (Boyde et al, 1986) and it has been suggested that breast carcinoma cells possess the capacity to recruit and stimulate osteoclasts by producing stimulatory factors (Boyde et al, 1986). Parathyroid hormone related peptide (PTHrP) is thought to be a major candidate factor produced by breast cancer cells which may promote osteoclastic activity at metastatic sites in bone (Powell et al, 1991).Bisphosphonates (BPs) are analogues of endogenous pyrophosphates in which a carbon atom replaces the central atom of oxygen. In vivo, bisphosphonates bind strongly to hydroxyapatite on the bone surface and are preferentially delivered to sites of increased bone formation or resorption. They are potent inhibitors of osteoclast-mediated bone resorption (Boonecamp et al, 1986) and are effective in lowering serum calcium concentrations in patients with hypercalcaemia of malignancy (Ryzen et al, 1985;Kanis et al, 1987). Bisphosphonates are also used in the treatment of Paget's disease of bone (Altman et al, 1973;Plasmans et al, 1978) and bone lesions associated with multiple myeloma (Berenson et al, 1996). The mechanisms by which bisphosphonates inhibit osteoclast-mediated bone resorption remain to be determined, but may involve inhibition of formation of osteoclasts from immature precursor cells (Boonecamp et al, 1986;Lowik et al, 1988;Hughes et al, 1989) and/or direct inhibition of resorption via induction of apoptosis in mature osteoclasts (Lowik et al, 1988;Hughes et al, 1995;Selander et al, 1996). More recently, several reports have indicated that bisphosphonates have direct effects on other cell types which may have important implications in the treatment of patients with cancer-induced bone disease. Treatment with intravenous pamidronate (Hortobagyi et al, 1998) and oral clodronate (Paterson et al, 1993) have been reported to reduce the frequency of skeletal complications in established bone disease. Oral clodronate has also been shown to decrease the frequency of skeletal metastases in women who had recurrent breast cancer but without bony involvement (Kanis et al, 1996). Moreover, oral clodronate has recently been shown to increase survival in women with breast cancer, when given at the time of initial diagnosis to patients who have bone marrow micrometastases at the time of surgery fo...

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Use of an Aqueous Soluble Tetrazolium/Formazan Assay for Cell Growth Assays in Culture

Cited by 1,379 publications

References 0 publications

SV40-derived vectors provide effective transgene expression and inhibition of HIV-1 using constitutive, conditional,and pol III promoters

SV40-derived vectors provide effective transgene expression and inhibition of HIV-1 using constitutive, conditional,and pol III promoters

Impaired homeostasis and phenotypic abnormalities in Prdx6−/−mice lens epithelial cells by reactive oxygen species: increased expression and activation of TGFβ

Bisphosphonates induce apoptosis in human breast cancer cell lines

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