Alkaline phosphatase in HT-29, a human colon cancer cell line: Influence of sodium butyrate and hyperosmolality

Herz, Fritz; Schermer, Alexander; Halwer, Murray; Bogart, Lee

doi:10.1016/0003-9861(81)90224-1

Cited by 78 publications

(30 citation statements)

References 45 publications

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“…This suggests that glycogen accumulation might be somehow involved in the process of differentiation when cells are grown with glucose. This hypothesis is further supported by other Glc' situations in which an enterocytic differentiation of human colon cells is associated with high values of glycogen content: Caco-2 cells, which are differentiated in Glc' medium store five times more glycogen than HT-29 cells (Rousset et al, 1979); the induction of some degree of enterocytic differentiation by sodium butyrate in cultured colon cancer cells (Kim et al, 1980;Herz et al, 1981) is associated with an increase in glycogen content (Dexter et a1.,1984); in the colon of human foetuses both sucrase-isomaltase Lacroix et al, 1984) and glycogen (Rousset et al, 1979) are present at midgestation, and they disappear concomitantly in the last stages of gestation. Any attempt to explain how glucose metabolism interferes with the differentiation of HT-29 cells would be Passage number 0 refers to passage 30 in Glcmedium.…”

Section: Discussionmentioning

confidence: 84%

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT‐29 selected for growth in sugar‐free medium and its inhibition by glucose

Zweibaum

Pinto

Chevalier

et al. 1985

Journal Cellular Physiology

313

193

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In order to study the effect of glucose on the differentiation of cultured human colon cancer cells, a subpopulation of HT-29 cells was selected for its capacity to grow in the total absence of sugar. These cells (Glc-cells) exhibit, after confluency, an enterocytic differentiation, in contrast to cells grown with glucose (Glc+ cells), which always remain undifferentiated. The differentiation is characterized by a polarization of the cell layer with apical brush borders and tight junctions, and by the presence of sucrase-isomaltase. The differentiation of Glc- cells is reversible: the addition of glucose to postconfluent cultures of Glc- cells results in an inhibiting effect on the expression of sucrase-isomaltase; switching growing cultures of Glc- cells to the Glc+ medium for several passages results in a progressive reversion to the undifferentiated state, which is completed after seven passages. The dedifferentiation process is associated with a parallel, passage-related, increase in the rates of glucose consumption and lactic acid production, and decreases of intracellular glycogen content, which return to the values of the undifferentiated original Glc+ cells. The values of these metabolic parameters are correlated, at each passage, with the degree of dedifferentiation of the cells. When these dedifferentiated cells, after having been cultured in Glc+ medium for 20 passages, are switched back to the Glc- medium, they readily grow without mortality, and reexpress the same enterocytic differentiation as the parent Glc- cells. These results show that the capacity of this subpopulation to grow and differentiate in the absence of sugar is a stable characteristic. They further suggest that glucose metabolism interferes with the program of differentiation of HT-29 cells.

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Section: Discussionmentioning

confidence: 84%

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT‐29 selected for growth in sugar‐free medium and its inhibition by glucose

Zweibaum

Pinto

Chevalier

et al. 1985

Journal Cellular Physiology

313

193

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“…The H-CaCo2 cells were washed and lysed with 0.25% sodium deoxycholate essentially as described by Herz et al [33]. ALP activity was determined using the Sigma Diagnostics ALP reagent (No.…”

Section: Alkaline Phosphatase Activitymentioning

confidence: 99%

Peptides from water buffalo cheese whey induced senescence cell death via ceramide secretion in human colon adenocarcinoma cell line

Simone¹,

Ferranti²,

Picariello³

et al. 2010

Molecular Nutrition Food Res

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“…Attached and floating cells were washed and lysed with 0.25% sodium deoxycholate essentially as described by Herz et al (1981). ALP activity was determined using the Sigma Diagnostics ALP reagent (No.…”

Section: Alkaline Phosphatase Activitymentioning

confidence: 99%

“…In particular, we addressed the question as to whether the TGFb 1 -induced apoptosis seen in the adenoma cell line PC/BH/C1 is via a terminal differentiation pathway or potentially by a differentiation-independent pathway, for example, due to conflicting growth signals (Askew et al, 1991;Evan et al, 1992;Shi et al, 1992). We examined alkaline phosphatase activity, a well-documented parameter of the degree of colonic epithelial differentiation (Yamomoto and Yasuda, 1973;Herz et al, 1981;Chung et al, 1985;Henthorn et al, 1988). Furthermore, we have used E-cadherin protein expression as an additional marker of colonic cell differentiation.…”

Section: Introductionmentioning

confidence: 99%

Butyrate- but not TGFβ1-induced apoptosis of colorectal adenoma cells is associated with increased expression of the differentiation markers E-cadherin and alkaline phosphatase

1997

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Sodium butyrate and transforming growth factor b (TGFb 1 ) are growth inhibitory to colonic adenoma cell lines. Butyrate induces apoptosis, whereas in some adenoma cell lines, TGFb 1 can be growth inhibitory without apoptosis. In this report, we show that the adenoma cell line PC/BH/C1 undergoes apoptosis in response to TGFb 1 . Butyrate induced cell death is preceded by the induction of two markers of colonic differentiation ± alkaline phosphatase (ALP) activity and E-cadherin protein expression. However, TGFb 1 -induced apoptosis was not accompanied by induction of these differentiation markers. It is possible that the apoptosis induced by TGFb 1 in the adenoma cell line PC/BH/C1 is due to conflicting signals, as downregulation of c-myc protein in response to TGFb 1 occurs only slowly in this cell line. Development of resistance to TGFb 1 in colonic tumours may involve two separate stages ± resistance to growth inhibition and resistance to TGFb 1 -induced apoptosis. Our results indicate that sodium butyrate induces apoptosis via differentiation, but TGFb 1 induces apoptosis by a differentiationindependent mechanism. As for butyrate, the induction of Ecadherin expression is a potentially important chemopreventative action, since increased E-cadherin expression has been correlated with decreased metastatic potential. This is the first report of induction of E-cadherin by a naturally occurring factor in the diet. Butyrate may reduce tumour growth and invasion, not only as a result of the induction of apoptosis, but also through increased expression of E-cadherin.

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Alkaline phosphatase in HT-29, a human colon cancer cell line: Influence of sodium butyrate and hyperosmolality

Cited by 78 publications

References 45 publications

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT‐29 selected for growth in sugar‐free medium and its inhibition by glucose

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT‐29 selected for growth in sugar‐free medium and its inhibition by glucose

Peptides from water buffalo cheese whey induced senescence cell death via ceramide secretion in human colon adenocarcinoma cell line

Butyrate- but not TGFβ1-induced apoptosis of colorectal adenoma cells is associated with increased expression of the differentiation markers E-cadherin and alkaline phosphatase

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