Sodium butyrate alters the response of a human colon carcinoma cell line to transforming growth factor-β1

Lewis, Laurie R.; Levine, Alan E.

doi:10.1016/0304-3835(92)90086-b

Cited by 5 publications

(3 citation statements)

References 16 publications

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“…Similar to our observation with 1,25(OH) 2 D 3 , butyrate was found to sensitize these cells to growth inhibition by TGF-␤1 (24,42). It was suggested that butyrate might alter the expression of proteins that mediate TGF-␤1 responses in these cells, but the signal transduction elements involved in these processes were not identified.…”

Section: Discussionsupporting

confidence: 78%

“…With regard to sensitization to TGF-␤1 growth inhibition by other agents, previous studies have demonstrated that another differentiating agent, the shortchain fatty acid butyrate, like 1,25(OH) 2 D 3 , induced the maturation and inhibited the cell growth of several colon cancer cell lines, including Caco-2 cells (24,42). Similar to our observation with 1,25(OH) 2 D 3 , butyrate was found to sensitize these cells to growth inhibition by TGF-␤1 (24,42).…”

Section: Discussionmentioning

confidence: 99%

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Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)₂D₃

Chen

Davis

Sitrin

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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Growth of Caco-2 and many cancer cells is inhibited by 1,25(OH)2D3. Whereas TGF-β1 inhibits normal colonic epithelial cell growth, most human colon cancer-derived cells, including Caco-2 and SW480 cells, are resistant to it. The mechanisms underlying these antiproliferative actions and resistance to TGF-β growth inhibition are largely unknown. We observed that 1,25-dihydroxyvitamin D3[1,25(OH)2D3] sensitized Caco-2 and SW480 cells to TGF-β1 growth inhibitory effects. Versus 1,25(OH)2D3 alone, the combination of 1,25(OH)2D3 and TGF-β1 significantly reduced cell numbers. Also, the amount of active TGF-β1 was increased (∼4-fold) by this secosteroid in conditioned media from Caco-2 cells. The 1,25(OH)2D3 increased the expression of IGF-II receptors (IGF-IIR), which facilitated activation of latent TGF-β1, and was found to activate TGF-β signaling in Caco-2 cells. By using neutralizing antibodies to human TGF-β1, we showed that this cytokine contributes to secosteroid-induced inhibition of Caco-2 cell growth. Also, 1,25(OH)2D3 was found to enhance the type I TGF-β receptor mRNA and protein abundance in Caco-2 cells. Whereas the 1,25(OH)2D3-induced sensitization of Caco-2 cells to TGF-β1 was IGF-IIR independent, the type I TGF-β1 receptor was required for this sensitization. Thus 1,25(OH)2D3 treatment of Caco-2 cells results in activation of latent TGF-β1, facilitated by the enhanced expression of IGF-IIR by this secosteroid. Also, 1,25(OH)2D3 sensitized Caco-2 cells to growth inhibitory effects of TGF-β1, contributing to the inhibition of Caco-2 cell growth by this secosteroid.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)₂D₃

Chen

Davis

Sitrin

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Antibodies were raised and the and membrane-bound proteins such as the ligand to Fas/ expression of the proteins was studied. It was found that APO-1 receptor (Laster et al, 1988;Trauth et al, 1989;Itoh et al, 1991;Lin and Chou, 1992;Novelli et al, DAP-1 codes for a 15 kDa proline-rich basic protein, that DAP-2 is a structurally unique 160 kDa serine/threonine Immunostaining and biochemical fractionations revealed that the kinase is localized to the cytoskeleton in associ-protein kinase (therefore named DAP-kinase), and that DAP-3 codes for a 46 kDa protein that carries a potential ation with the microfilament system and defined a region downstream of the first P-loop motif which contributes to ATP/GTP binding motif Kissil et al, 1995).…”

mentioning

confidence: 99%

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

1997

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Kissil et al., 1995). Other laboratories adapted localized to the cytoskeleton, in association with the similar functional selection strategies and candidate genes microfilament system, and mapped a region within that mediate cell death induced by IL-3 deprivation or by the protein which is responsible for binding to the T-cell receptor activation were cloned including Requiem cytoskeleton. Several assays attributed a cell death (Gabig et al., 1994), ALG-2 and ALG-3 (Vito et al., 1996). function to the gene. Ectopic expression of wild-type Our method, called Technical Knock Out (TKO), was DAP-kinase induced the death of target cells, and the based on random inactivation of genes via introduction of killing property depended strictly on the status of the anti-sense cDNA expression libraries, prepared from a intrinsic kinase activity. Conversely, a catalytically mixture of non-treated and IFN-γ-treated cells. The genes inactive mutant that carried a lysine to alanine substituof interest were selected and cloned by virtue of the tion within the kinase domain, displayed dominantdefined phenotypic change-reduced susceptibility to the negative features and protected cells from interferoncytokine-induced cell death-which resulted from their γ-induced cell death. DAP-kinase is therefore a novel inactivation. HeLa cells, transfected with Epstein-Barr cytoskeletal-associated cell death serine/threonine virus (EBV)-based vectors carrying anti-sense cDNA kinase whose activation by Ca 2⍣ /calmodulin may be libraries, were subjected to positive selection of cells that linked to the biochemical mechanism underlying the survived in the continuous presence of IFN-γ. The rescued cytoskeletal alterations that occur during cell death.plasmids that were positively scored in a second round of Keywords: calcium/calmodulin/cytoskeleton/programmed transfection carried six non-overlapping groups of cDNA cell death/serine-threonine kinase fragments. Sequence analysis indicated that five of them corresponded to novel genes: DAPs 1-5 . The sixth gene was identical to a known aspartic protease, i.e. cathepsin D, the participation of which was

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Transforming growth factor β and cancer

Nørgaard

Hougaard

Poulsen

et al. 1995

Cancer Treatment Reviews

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Sodium butyrate alters the response of a human colon carcinoma cell line to transforming growth factor-β1

Cited by 5 publications

References 16 publications

Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)₂D₃

Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)₂D₃

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

Transforming growth factor β and cancer

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Sodium butyrate alters the response of a human colon carcinoma cell line to transforming growth factor-β1

Cited by 5 publications

References 16 publications

Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)2D3

Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)2D3

DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

Transforming growth factor β and cancer

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Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)₂D₃

Transforming growth factor-β1 signaling contributes to Caco-2 cell growth inhibition induced by 1,25(OH)₂D₃