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PubMed2006

Valproic acid and butyrate induce apoptosis in human cancer cells through inhibition of gene expression of Akt/protein kinase B.

BACKGROUND: In eukaryotic cells, the genomic DNA is packed with histones to form the nucleosome and chromatin structure. Reversible acetylation of the histone tails plays an important role in the control of specific gene expression. Mounting evidence has established that histone deacetylase inhibitors selectively induce cellular differentiation, growth arrest and apoptosis in variety of cancer cells, making them a promising class of anticancer drugs. However, the molecular mechanisms of the anti-cancer effects of these inhibitors have yet to be understood. RESULTS: Here, we report that a key determinant for the susceptibility of cancer cells to histone deacetylase inhibitors is their ability to maintain cellular Akt activity in response to the treatment. Also known as protein kinase B, Akt is an essential pro-survival factor in cell proliferation and is often deregulated during tumorigenesis. We show that histone deacetylase inhibitors, such as valproic acid and butyrate, impede Akt1 and Akt2 expression, which leads to Akt deactivation and apoptotic cell death. In addition, valproic acid and butyrate induce apoptosis through the caspase-dependent pathway. The activity of caspase-9 is robustly activated upon valproic acid or butyrate treatment. Constitutively active Akt is able to block the caspase activation and rescues cells from butyrate-induced apoptotic cell death. CONCLUSION: Our study demonstrates that although the primary target of histone deacetylase inhibitors is transcription, it is the capacity of cells to maintain cellular survival networks that determines their fate of survival.

Apoptosis↗
PubMed2003

Nicotinic induction of preproenkephalin and tyrosine hydroxylase gene expression in butyrate-differentiated rat PC12 cells: a model for adaptation to gut-derived environmental signals.

Accelerated maturation of peripheral sympathoadrenal transmitter levels and function occurs at 7-10 postnatal days in the rat. This event is temporally disconnected from the timing of major changes in physiologic stimuli evident after the birthing process (i.e. temperature, oxygen, sound, light, etc.). Colonization of the gut, fermentation of carbohydrates, and production of short-chain fatty acids (e.g. butyrate) mirrors this postnatal time course. In this report, we examined the interaction between butyrate differentiation of rat pheochromocytoma cells and cholinergic-nicotinic induction of the neuropeptide (enkephalin) and catecholamine-related biosynthetic enzymes (tyrosine hydroxylase, dopamine beta-hydroxylase, phenylethanolamine N-methyltransferase). Our results show that butyrate induces both preproenkephalin and tyrosine hydroxylase mRNA through a proximal promoter region and that this regulatory step is time and dose dependent. Moreover, there is an additional interaction with cholinergic-nicotinic inducible mechanisms consistent with classically described transsynaptic cholinergic regulation of these genes. Dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase promoters were not affected by butyrate treatment. We speculate that colonization of the human gut (along with the attendant fermentation of enteral carbohydrates to short-chain fatty acids) may represent a mechanism through which environmental signals affect postnatal maturation of sympathoadrenal transmitter systems.

Animals↗
PubMed2000

Dietary butyrate inhibits NMU-induced mammary cancer in rats.

Butyrate has been proposed as an antineoplastic agent, leading to the inhibition of tumorigenesis. The purpose of this study was to examine butyrate, supplied as tributyrin (Tbn) or as a natural component of anhydrous milk fat (AMF), on the development of nitrosomethylurea-induced mammary tumors in female Sprague-Dawley rats. Diets were 1) semipurified rodent diet (AIN-93) with high fat [20% sunflower seed oil (SSO), control], 2) SSO diet with Tbn added at 1%, 3) SSO diet with Tbn added at 3%, and 4) 19% AMF with 1% SSO diet, which contained butyrate equivalent to the 1% Tbn diet. These diets were fed ad libitum from weaning at 21 days of age, and at 24 days of age each rat was injected with nitrosomethylurea (50 mg/kg body wt i.p.). At any one period, there was a relative risk increase of 88% (p < 0.05) that rats in the SSO diet group would develop a mammary tumor compared with those in the AMF diet group. The addition of 1% and 3% Tbn to SSO diets reduced the tumor incidence by 20% and 52%, respectively, in comparison to SSO alone (p < 0.05). There was a linear inverse relationship between Tbn concentration and rats developing a tumor. From 89 days to the end of the experiment, rats fed the diet containing 3% Tbn showed a significantly lower multiplicity of palpable tumors (50% less at Day 118, p < 0.05) than SSO-fed rats. These results indicate that although the AMF diet was effective, particularly early in reducing mammary tumorigenesis, the 3% Tbn diet produced a sustained reduction of tumor multiplicity relative to the control (SSO) group. An inhibitory influence of butyrate on mammary tumorigenesis against a background of high polyunsaturated fat diet has been demonstrated in this animal model of breast cancer.

Alkylating Agents↗
PubMed1976

Ultrastructural and enzymic modulation of HeLa cells induced by sodium butyrate and the effects of cytochalasin B and colcemid.

Sodium butyrate causes HeLa cells to assume an elongated and jagged shape. Ultrastructurally this change is associated with the formation of bundles of microfilaments. Desmosomes were present between adjacent cells. No increase in microtubules was observed in the butyrate-treated cells. Butyrate induces an increase in the activity of 2 membrane-bound enzymes, alkaline phosphatase and 5'-nucleotidase; however, the activity of a third membrane enzyme, acetylcholine esterase, is reduced. The activities of the several other enzymes with different subcellular localizations are not significantly increased. Colcemid and cytochalasin B prevent or reverse the butyrate-mediated change in HeLa cell morphology and also partially inhibit the induction of alkaline phosphatase activity in these cells. The effect of cytochalasin B on alkaline phosphatase induction may be caused by a reduction in protein synthesis produced by this fungal metabolite.

Acid Phosphatase↗
PubMed2000

Up-regulation of E-cadherin and I-catenin in human hepatocellular carcinoma cell lines by sodium butyrate and interferon-alpha.

Human E-cadherin is a homophilic cell adhesion molecule and its expression is well preserved in normal human hepatocytes; a decrease in its expression has been observed in poorly differentiated hepatocellular carcinoma cells. We examined the alteration of E-cadherin and catenin expressions caused by differentiation inducers in human hepatocellular carcinoma cells. Hepatocellular carcinoma cell lines, HCC-T and HCC-M, were cultured with all-trans retinoic acid (ATRA), dexamethasone (DEX), sodium butyrate, and interferon-alpha. E-cadherin expression was only up-regulated by butyrate and interferon-alpha (IFN-alpha) in both cell lines, studied by means of fluorescence immunostaining and flow cytometry. The localization of E-cadherin staining was shown at their cell membrane. According to the increase in E-cadherin expression, beta-catenin expression appeared at the cell membrane of both cell lines when treated with butyrate and IFN-alpha. Such an appearance was not observed when cells were treated with ATRA and DEX. Western blotting showed that alpha- and y-catenin expression was not changed, while only the expression of beta-catenin increased. Beta-catenin oncogenic activation as a result of amino acid substitutions or interstitial deletions within or including parts of exon 3, which has been demonstrated recently, was not detected in these cell lines by direct deoxyribonucleic acid sequencing. These results suggest that the expression and interaction between E-cadherin and wild-type beta-catenin are potentially modulated by butyrate and IFN-alpha, and that these two agents are potent inhibitors of hepatocellular carcinoma cell invasion and metastasis.

Amino Acid Substitution↗
PubMed2001

Simple gas chromatography analysis of faecal butyrate: application to patients at risk of pouchitis.

In spite of the fact that pouchitis is the most frequently occurring and troublesome complication found in patients treated by ileo-anal anastomosis for ulcerative colitis, no biological marker currently exists to monitor the outcome of the disease. Since it has been noted faecal butyrate is reduced in patients with pouchitis, we developed a simple gas chromatography method to quantify butyrate in faecal water. This test is based on diethyl ether extraction with the use of methacrylic acid as an internal standard. We demonstrated that butyrate was effectively measured when this technique was applied to eleven patients with ileal-pouch anal anastomosis within the first year after the closure of their ileostomy. We also observed a noticeable reduction in the concentration of butyrate in patients who went on to develop a pouchitis.

Adult↗
PubMed2002

Na+/H+ exchange in primary, secondary and n-butyrate-treated cultures of ruminal epithelial cells: short communication.

Rate of amiloride-sensitive Na+ uptake into cultured rumen epithelial cells was studied in order to clarify the influence of culture conditions on Na+/H+ exchange (NHE). Cell cultures were exposed to Na-n-butyrate or not for seven days or subcultured. On the 14th day of culturing, primary cell cultures without butyrate exposure showed both non-stratified and stratified growth. Na-n-butyrate treated 14-day-old cultures and 3-day-old subcultures contained mostly non-stratified, i.e. non-keratinised cells. Both n-butyrate treatment and subculturing increased total and amiloride-sensitive Na+ uptake. Our results indicate that Na+ uptake via NHE is determined by the amount and the ratio of non-stratified (non-keratinised) cells.

Amiloride↗
PubMed2000

Effect of sodium butyric acid, sodium valerianic acid, and osmolarity on contractility of specimens of intestinal wall obtained from the cecum and spiral colon of healthy cows.

OBJECTIVE: To compare the effect of various concentrations of sodium butyric acid and sodium valerianic acid, as well as various osmolarities, on contractility of ex-vivo intestinal wall specimens obtained from the cecum and spiral colon of each of several healthy cows. SAMPLE POPULATION: Full-thickness preparations of intestinal wall, dissected parallel to the longitudinal smooth muscle layers, harvested from freshly slaughtered healthy cows. PROCEDURE: Specimens of intestinal wall were incubated for 5 minutes with various concentrations of sodium butyric acid and sodium valerianic acid as well as various osmolar concentrations of NaCl, using a crossover design. Isometric contractions were induced 7 times with carbachol (CH; 5 X 10(-6) mol/L). Contractility was defined as the maximum amplitude of contraction and the amplitude of contraction 2 minutes after addition of CH. RESULTS: Repeated addition of CH did not result in a significant effect on contractility of specimens from the cecum and spiral colon. Contractility after addition of CH was not significantly affected by prior incubation with various concentrations of sodium butyric acid or sodium valerianic acid or after an increase of osmolarity. Maximum amplitude of contraction was significantly higher in specimens from the spiral colon, compared with specimens from the cecum. CONCLUSIONS: Increases in concentrations of sodium butyric acid or sodium valerianic acid and increases in osmolarity did not inhibit contractility of intestinal wall specimens from the cecum and spiral colon of a group of healthy cows.

Animals↗
PubMed2003

Effects of butyrate on apoptosis in the pig colon and its consequences for skatole formation and tissue accumulation.

Evidence exists that butyrate inhibits apoptosis of colon crypt cells in vivo so that less tryptophan from cell debris is available for skatole formation by microbes in the pig colon. In this study, potato starch containing a high proportion of resistant starch was fed to test the hypothesis that increased butyrate formation will occur in the colon and contribute to reduced epithelial cell apoptosis, thus leading to reduced skatole formation and absorption. Two groups of six barrows were provided with catheters in the jugular vein and fed either a ration with pregelatinized starch (high ileal digestibility; controls) or potato starch (low ileal digestibility; PS) as the main carbohydrate. All pigs were fed 31 MJ of metabolizable energy and 381 g of crude protein per day. The controls were fed for 19 d. The PS group received the same control ration for 10 d, and then changed to the PS ration. The total feeding period of PS consisted of a 5 d adaptation period followed by another 19 d. In the continously sampled feces, pH, short chain fatty acids, and skatole were determined. Skatole was additionally measured in blood plasma that was sampled daily. After killing barrows at the end of the feeding period, fat tissue for skatole measurement and colon tissue for histological quantification of mitosis and apoptosis were obtained. Feeding potato starch led to a rapid 2.2 fold increase of fecal butyrate when compared both with the control period of the PS group and the control group (P < 0.001). PS feeding resulted in a decrease in pH from 7.3 to 5.3 (P < 0.001) and apoptosis from 2.06 cells/crypt to 0.90 cells (P < 0.01), whereas there was no change in mitosis. Consequently, skatole decreased both in feces (controls vs PS group: 120.0 vs 1.9 microg/g; P < 0.001) and in blood plasma (1.6 vs 0.2 ng/mL; P < 0.001). The mean concentration of skatole in fat tissue was 167 ng/g tissue in controls, and below the detection limit (0.8 ng/g) in the PS group (P < 0.001). It is concluded that butyrate-dependent inhibition of apoptosis in the colon due to potato starch feeding efficiently inhibits skatole production in barrows. Because of the depressed skatole levels, improved sensory quality of pork is possible.

Animal Feed↗
PubMed2004

Feeding lactose increases ruminal butyrate and plasma beta-hydroxybutyrate in lactating dairy cows.

Ruminal fermentation of lactose increases molar proportions of butyrate, which is metabolized by the ruminal epithelium to beta-hydroxybutyrate (BHBA). To determine the effects of dietary whey, and specifically lactose, on concentrations of ruminal and blood volatile fatty acids (VFA) and blood BHBA, 8 Holstein and 4 Brown Swiss multiparous cows (210 +/- 33 d in milk) were blocked by breed and randomly assigned to one of three 4 x 4 Latin squares. Treatments were control (CON; 7.1% of dietary dry matter [DM] as cornstarch), liquid whey (WHEY; 9.4% of diet DM) containing 70% lactose on a DM basis, low lactose (LOLAC; 7.1% lactose), or high lactose (HILAC; 14.3% lactose). Diets contained 53% forage as corn silage, alfalfa hay, and grass hay (DM basis) and a corn and soybean meal-based concentrate. Average dietary percentage of crude protein and energy density (Mcal/kg net energy for lactation) were 16.8 and 1.47, respectively. Feeding lactose increased DM intake. Milk production and composition were not affected by diet with the exception of decreased urea nitrogen in milk from cows fed lactose. Greater proportions of ruminal propionate were observed in cows fed CON relative to those fed WHEY and LOLAC. Increasing dietary lactose increased proportions of ruminal butyrate and decreased acetate and branched-chain VFA. Concurrent with the increase in ruminal butyrate concentrations, there was an increase in plasma BHBA as lactose in the diet increased. Concentrations of VFA in plasma were not affected by diet with the exception of the branched-chain VFA, which were increased in cows fed LOLAC compared with WHEY. These data indicate lactose fermentation increases proportions of ruminal butyrate and plasma BHBA in lactating dairy cows; however, the observed increase in plasma BHBA is not sufficient to subject cows to ketosis.

3-Hydroxybutyric Acid↗
PubMed1978

Rumen epithelial cell proliferation accelerated by rapid increase in intraruminal butyrate.

Two pairs of adult castrated male sheep were given intraruminally 2 g/kg body weight per day of sodium n-butyrate rapidly 10 s at noon or slowly over 20 to 24 h from noon in four trials in which they received only mixed minerals and water ad libitum. Their ruminal papillae were biopsied just before each administration and 24 h after the final administration. Mitotic indices of the epithelial cells were observed. Mitotic indices were lower than .48% before butyrate administration. In sheep rapidly administered butyrate, mitotic indices increased to 1.29%, 2.33%, 2.65%, and 1.84% in 1 day after the first administration in four trials and tended to decline on later days. In sheep slowly administered butyrate, mitotic indices stayed lower than .50% and did not show significant fluctuations. Our data support our hypothesis that an increase in the rate of intraruminal production of volatile fatty acids promotes proliferation of epithelial cells of the organ.

Animals↗
PubMed1991

Effects of ketones, acetate, butyrate, and glucose on bovine lymphocyte proliferation.

Blood leukocytes from age-matched heifers were used to determine effects of ketones, acetate, butyrate, and glucose on in vitro lymphocyte proliferation. Lymphocytes stimulated with concanavalin A, phytohemagglutinin-P, or pokeweed mitogen were cultured in the presence or absence of beta-hydroxybutyrate, acetoacetate, acetone, acetate, butyrate, and glucose. Only supraphysiological levels of beta-hydroxybutyrate inhibited proliferation in cultures of mitogen-stimulated lymphocytes, whereas mixtures of beta-hydroxybutyrate and acetoacetate at levels seen in severe ketosis stimulated concanavalin A and phytohemagglutinin-P-driven proliferation. Because acetoacetate was a lithium salt, lithium chloride served as a negative control. Results suggest the enhanced proliferation by cultures containing lithium acetoacetate was due to lithium, not acetoacetate. Butyrate (at concentrations greater than seen in bovine plasma) and acetate at normal levels inhibited proliferation. Concanavalin A- and pokeweed-mitogen-driven proliferation was greater in cultures containing lower glucose levels, but acetate added to cultures containing low glucose inhibited concanavalin A-stimulated proliferation. Proliferation by pokeweed mitogen-stimulated cultures containing acetate, beta-hydroxybutyrate, and acetoacetate was suppressed at the lower concentrations of glucose tested. In conclusion, ketones, butyrate, and glucose at concentrations occurring in vivo had minimal effects on bovine lymphocyte proliferation in vitro. Levels of acetate associated with ketosis suppressed lymphocyte function and may alter immune responsiveness in vivo.

Acetates↗
PubMed1998

Decreased phospholipase A2 activity in butyrate differentiated HT29 cells.

Our earlier work has shown that in butyrate differentiated colonic HT29 cells, there is an alteration in phospholipid composition as compared to control. To know more about these changes, butyrate treated and control cell homogenates were incubated in presence of calcium and phospholipids were analyzed. It was observed that incubation with calcium was associated with increase in lysophosphatidylcholine (lysoPC) and free fatty acids and the increase was much higher in control as compared to butyrate treated cells. There was no alteration in lysoPC content. These products are formed by the action of phospholipase A2 (PLA2) which is activated by calcium and suggests that butyrate-induced differentiation is associated with decrease in PLA2 activity.

Butyrates↗
PubMed2000

Involvement of Gialpha2 in sodium butyrate-induced erythroblastic differentiation of K562 cells.

The chronic myelogenous leukaemia cell line K562 can be triggered in culture to differentiate along the erythrocytic pathway in response to a variety of stimulatory agents. In the presence of sodium butyrate, these cells differentiate to erythroblasts and acquire the capability to synthesize haemoglobin. We used this cell system to study alterations in the levels of several G-protein subunits during the cell differentiation programme and to assess the involvement of G(i)alpha2 in this process. Western immunoblot analysis revealed the presence of G(s)alpha1, G(s)alpha2, G(i)alpha2, G(q)alpha, Galpha(12), Gbeta1 and Gbeta2 in K562 cells. G(o)alpha, G(z)alpha, Galpha(13) and Galpha(16) were not detected. Although the levels of several G-protein subunits were altered after treatment with sodium butyrate, the most striking change was the robust increase in the levels of G(i)alpha2, which was accompanied by an increase in the mRNA for G(i)alpha2. Inactivation of G(i)alpha2 by adding Bordetella pertussis toxin to the cultures inhibited erythroblastic differentiation by as much as 62%, as measured by haemoglobin accumulation. Furthermore, the addition of an oligonucleotide anti-sense to G(i)alpha2 inhibited the sodium butyrate-induced robust increase in G(i)alpha2 levels, decreasing it to the basal levels seen in control cells; this treatment decreased the erythroblastic differentiation of the cells (as measured by haemoglobin expression) by 50%. Taken together, these findings imply that increased levels of G(i)alpha2 contribute to the sodium butyrate-induced erythroblastic differentiation of K562 cells.

Butyrates↗
PubMedDate not supplied

Pretreatment of endometrial carcinoma cell lines with butyrate results in upregulation of Bax and correlates with potentiation of radiation induced cell kill.

BACKGROUND: Endometrial carcinoma is the most common gynecologic malignancy. Surgery has been the standard therapy for stage I and II endometrial carcinoma and radiation therapy either before or after surgery has been used to improve local control especially for high grade lesions. We have used Sodium Butyrate (BA) in order to examine whether endometrial carcinoma cells can be rendered more sensitive to radiation therapy. METHODS: Endometrial carcinoma cells in culture were pretreated with sodium butyrate and then irradiated. Clonogenic survival assay was used to determine percentage of surviving cells. Changes in Bax and Bcl-2 protein levels were determined by Western blot analyses. Effect of Bcl-2 overexpression on induction of Bax in response to butyrate pretreatment was studied in cells transfected with Bcl-2. RESULTS: A 24 h pretreatment of SKUT2 and Hec-1A cells with BA has an additive effect with radiation. Analysis of pro and anti-apoptotic protein levels revealed that the 24 h pretreatment with BA resulted in increased expression of the proapoptotic protein Bax which correlated with potentiation of radiation induced cell kill. Treatment of cells over expressing Bcl-2 with BA did not show induction of Bax suggesting that higher levels of Bcl-2 can block butyrate induced increase in levels of Bax. CONCLUSIONS: Use of BA at lower than toxic doses to upregulate the proapoptotic potential of cancer cells may be useful in an adjuvant or neoadjuvant setting but its success may depend upon the intrinsic Bcl-2 levels in the tumor.

Adenocarcinoma↗
PubMed2001

Butyrate induced alterations during development of the strain ln(1)BM2(reinverted) of Drosophila melanogaster.

The polytene male X chromosome of D. melanogaster, has a unique morphology, which is correlated with the property of increased transcription of the sex-linked genes of the male X chromosome. This ensures equalization of X-linked gene products between males (XY) and females (XX). Till date, an invariable correlation between the structure and transcription of the male X chromosome has been reported. However, the strain In(1)BM2(reinverted) of D. melanogaster presents a caveat to this invariable correlation. In this strain, although the male X chromosome appears puffy and diffuse, the transcription remains at the wild type level. This observation suggests the perturbation in the function of a regulator that controls the structure of the male X chromosome. In this report the response of the strain to butyrate, an inhibitor of histone deacetylase, has been studied, with specific reference to development, sex ratio and chromosome morphology of the strain. Two important conclusions arise from these experiments : (a) exposure to butyrate has more severe consequences on the development of the mutant strain and on the survival of females. (b) rearing on butyrate induced a temporal series of structural alteration of the polytene chromosome of the wild type, with the male X chromosome being most vulnerable to structural changes. The butyrate-interaction of In(1)BM2(reinverted) together with our current biochemical analyses of a chromosome coiling protein recovered from this strain, provide data for a working hypothesis explaining the sex and chromosome specific alteration of the structure of the male X chromosome of In(1)BM2(reinverted).

Animals↗
PubMed2001

Post-transcriptional effects of interleukin-3, interferon-gamma, erythropoietin and butyrate on in vitro hemoglobin chain synthesis in congenital hemolytic anemia.

BACKGROUND AND OBJECTIVES: Various agents modulate hemoglobin synthesis. In vitro modulation of translation in hemoglobin chain synthesis was analysed in patients with congenital hemolytic anemia (n=32) and healthy controls (n=17). DESIGN AND METHODS: Enriched reticulocytes were co-incubated with (3)H-leucine and cytokines or butyrate. Reversed-phase chromatography enabled separation of alpha-, beta- and gamma-globin chains. Globin chain synthesis was calculated from measured (3)H-leucine incorporation. Transferrin, erythropoietin, interleukin-3 and interferon-gamma receptors were detected by flow cytometry. Reverse-transcription polymerase chain reaction (RT PCR) was used to demonstrate changes of RNA stability. RESULTS AND DISCUSSION: Interleukin-3, interferon-gamma and butyrate caused a significant 2-fold increase (range 1.8-2.4; p<0.01) of the alpha- and beta-chain synthesis in congenital hemolytic anaemias. Analysis of gamma-globin chain synthesis revealed a lower, i.e. 1.4 fold increase (range 1.32 to 1.41; p<0.03). The absolute amount of globin synthesis was calculated to be 2.9 x 10(-12) g/reticulocyte/24h. After incubation with interleukin-3 the absolute additional synthesis of the alpha-globin chain reached 1.31 x 10(-12) g/reticulocyte/24h, of the beta-globin chain, 1.15 x 10(-12) g/reticulocyte/24h and of the gamma-globin chain, 0.26 x 10(-12) g/reticulocyte/24h. Butyrate and interferon-gamma had no or even an inhibiting effect on reticulocytes from normal controls, while interleukin-3 stimulated alpha- and gamma-chain synthesis (1.4 and 2.4 fold, respectively; p<0.03) suggesting an increase of fetal hemoglobin (HbF). Erythropoietin showed no stimulating influence. Membrane associated interleukin-3 receptors were detected in 0.78+/-0.14%, and interferon-gamma receptors in 0.1+/-0.015% of the red cells. Erythropoietin receptors were extremely rare (0.05+/-0.015%). The expression of transferrin receptors (CD71) correlated with the extent of globin chain stimulation. The alpha-, and beta-globin mRNA content of the reticulocytes after interleukin-3 incubation, as measured by RT-PCR, increased. INTERPRETATION AND CONCLUSIONS: Hemoglobin chain synthesis could be modulated post-transcriptionally by interleukin-3, interferon-gamma and butyrate. Transferrin receptor and globin RNA stability might be involved in this phenomenon.

Adolescent↗
PubMed2001

[The effects of sodium butyrate on proliferation, differentiation and apoptosis in immortalized esophageal epithelial cells].

OBJECTIVE: To study the effects of sodium butyrate on proliferation, differentiation and apoptosis of immortalized esophagus epithelial cells. METHODS: SHEE, an immortalized human fetal esophageal epithelial cell line induced by HPV18 E6E7, was cultivated in culture flasks and 24-well plates. Two experiment groups of cultured cells were treated with 1 and 5 mmol/L of sodium butyrate respectively for 4 days, and one group of untreated cells set aside as control. The numbers of cloned cells were calculated. The ultra-structure of SHEE cells was examined by transmission electron microscopy (TEM). The cell cycle and number of apoptotic cells were measured by flow cytometry, Ki-67 and cytokeratin of cells were detected by immunohistochemistry method and F-actin of cells labeled with phalloidin was examined by laser confocal scanning microscopy. RESULTS: Colony formations showed a significant decrease in the 2 experiment groups after 4 days of culture (P < 0.01). In the 1 mmol/L group, the cells at S phase were diminished and arrested at G(0)/G(1) phase. Compared with control group, Ki-67 positive cells were found decreased, while F-actin and cytokeratin were increased. Apoptotic cells in 5 mmol/L group were increased markedly. CONCLUSIONS: Sodium butyrate may induce SHEE cells growth arrest, differentiation and apoptosis. The effects depend on sodium butyrate concentration and time of exposure. Whether it can be used in combination with other anticancer drugs should be further studied.

Actins↗