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PubMed2003

Upregulation of activin A gene by butyrate in human colon cancer cell lines.

Activin A has been reported to play a role in the progression of colorectal cancer. Because dietary fiber protects against colorectal cancer, we hypothesized that butyrate, a fermentation product of dietary fiber, may affect the expression of activin A in colon cancer cells. Semiquantitative RT-PCR demonstrated that the activin A gene was upregulated by sodium butyrate in the human colon cancer cell lines HT-29 and Caco-2 in a concentration- and time-dependent manner. However, the activin A gene did not respond to sodium butyrate in the human normal colonic cell line FHC, rat normal intestinal epithelial cell (IEC) line IEC-6, and the explant of rat colon. Flow cytometry and agarose gel electrophoresis of genomic DNA revealed that cell cycle arrest and apoptosis were induced by sodium butyrate but not exogenous activin A in HT-29 cells, indicating that activin A could not act as an autocrine factor in colon cancer cells. By assuming that activin A promotes colorectal cancer spread as a paracrine factor, our findings suggest that butyrate could act as a tumor promoter in some circumstances.

Activins↗
PubMed2004

Butyrate increases apoptosis induced by different antineoplastic drugs in monocytic leukemia cells.

BACKGROUND: Apoptosis is an essential form of cell death, the failure of which can lead to cancer development. Cancer including leukemia is usually treated with chemotherapeutic drugs that can be effective, but frequently problems are encountered that impair the success of the treatment. Butyrate is a short-chain fatty acid that can have many effects on different cells, including apoptosis. METHODS: The effect of a combination treatment with butyrate and antineoplastic agents Ara-C, etoposide and vincristine is evaluate on the leukemic cell line THP-1. RESULTS: We show that butyrate increased apoptosis induced by the three agents as seen by measurement of DNA content, annexin exposure and morphological characteristics. We also demonstrate that the process of apoptosis induced by butyrate and chemotherapeutic drugs involves the participation of caspases and induced activation of caspase-3, -8 and -9. CONCLUSIONS: We believe that butyrate could be a promising therapeutic agent for the treatment of leukemia in combination with other antineoplastic drugs.

Amino Acid Chloromethyl Ketones↗
PubMedDate not supplied

Wheat bran decreases aberrant crypt foci, preserves normal proliferation, and increases intraluminal butyrate levels in experimental colon cancer.

BACKGROUND: Dietary wheat bran protects against colon cancer, but the mechanism(s) of this effect is not known. Butyrate, produced by colonic bacterial fermentation of dietary polysaccharides, such as wheat bran, induces apoptosis and decreases proliferation in colon cancer cell lines. Whether similar effects occur in vivo is not well defined. We hypothesized that wheat bran's antineoplastic effects in vivo may be mediated in part by butyrate's modulation of apoptosis and proliferation. METHODS: Male F344 rats were fed wheat bran-supplemented or an isocaloric, isonitrogenous fiber-free diet. Rats were treated with one dose of the carcinogen azoxymethane or vehicle with sacrifice after 5 days (tumor initiation); or two doses (days O and 7) with sacrifice after 56 days (tumor promotion). Study variables included fecal butyrate levels and the intermediate biomarkers of colon carcinogenesis, aberrant crypt foci (ACF), and changes in crypt cell proliferation and apoptosis. RESULTS: During tumor initiation, wheat bran produced greater apoptosis (p = .01), a trend toward less proliferation, and preserved the normal zone of proliferation (p = .01). At tumor promotion, wheat bran decreased the number of ACF (proximal colon, p = .005; distal colon, p = .047) and maintained the normal proliferative zone. The fiber-free diet shifted the zone of proliferation into the premalignant pattern in both studies. Wheat bran produced significantly higher fecal butyrate (p = .01; .004, .00001) levels than the fiber-free diet throughout the tumor promotion study. CONCLUSIONS: Wheat bran increased apoptosis and controlled proliferation during tumor initiation and resulted in decreased ACF. Wheat bran's antineoplastic effects occurred early after carcinogen exposure, and were associated with increased fecal butyrate levels.

Animals↗
PubMed2006

Butyrate induces profound changes in gene expression related to multiple signal pathways in bovine kidney epithelial cells.

BACKGROUND: Global gene expression profiles of bovine kidney epithelial cells regulated by sodium butyrate were investigated with high-density oligonucleotide microarrays. The bovine microarray with 86,191 distinct 60mer oligonucleotides, each with 4 replicates, was designed and produced with Maskless Array Synthesizer technology. These oligonucleotides represent approximately 45,383 unique cattle sequences. RESULTS: 450 genes significantly regulated by butyrate with a median False Discovery Rate (FDR) = 0 % were identified. The majority of these genes were repressed by butyrate and associated with cell cycle control. The expression levels of 30 selected genes identified by the microarray were confirmed using real-time PCR. The results from real-time PCR positively correlated (R = 0.867) with the results from the microarray. CONCLUSION: This study presented the genes related to multiple signal pathways such as cell cycle control and apoptosis. The profound changes in gene expression elucidate the molecular basis for the pleiotropic effects of butyrate on biological processes. These findings enable better recognition of the full range of beneficial roles butyrate may play during cattle energy metabolism, cell growth and proliferation, and possibly in fighting gastrointestinal pathogens.

Acetylation↗
PubMed2005

Effect of bile acids on butyrate-sensitive and -resistant human colon adenocarcinoma cells.

A controlled balance among cell proliferation, differentiation, and apoptosis is required for the maintenance of gastrointestinal mucosa; these processes are influenced by luminal components, such as butyrate and bile acids. Using butyrate-sensitive (BCS-TC2) and butyrate-resistant (BCS-TC2.BR2) human colon carcinoma cells, we wanted to establish whether colon carcinoma cells that acquire resistance to butyrate-induced apoptosis are also resistant to the cytotoxic effect of certain bile acids, contributing, in this way, to the progression of colon carcinogenesis. The effect of bile acids on BCS-TC2 cell viability is dose and time dependent and highly stereospecific. Quantification of the relative percentage of apoptotic cells and caspase-3 activity reveals that deoxycholic acid (DCA) and chenodeoxycholic acid (CDCA) induce apoptosis in BCS-TC2 cells. BCS-TC2.BR2 cells are consistently less sensitive to their cytotoxic effects, requiring concentrations to induce 50% inhibition (IC50) in cell viability of 740 microM and >1 mM for CDCA and DCA, respectively, compared with IC50 values of 310 and 540 microM for BCS-TC2 cells. DCA-treated BCS-TC2.BR2 cells show few apoptotic signs and no caspase-3 activation. On the other hand, CDCA-treated BCS-TC2.BR2 cells show caspase-3 activation and apoptotic features, although to a lower extent than BCS-TC2 cells. Our results, in an in vitro model system, point out that acquisition of butyrate resistance is accompanied by a partial resistance to the cytotoxic effects of bile acids, which may enhance the survival of tumorigenic cells.

Adenocarcinoma↗
PubMed2001

Comparative effects of chronic exposure to glucose or sodium butyrate on surfactant development in fetal rabbits.

BACKGROUND: Infants of diabetic mothers (IDM) often have delayed lung development and are thus at an increased risk of Respiratory Distress Syndrome (RDS). Both hyperglycemia and/or hyperinsulinemia have been implicated in this delay but the precise mechanism has not been clarified. Another metabolite, sodium butyrate, which is increased in IDM has been shown to decrease surfactant production in vitro but its effects on the development of the fetal lung surfactant system in vivo have not been studied. AIM: To investigate the in vivo effects of high glucose and sodium butyrate treatment on maternal and fetal glucose and insulin levels and on fetal lung surfactant maturation using timed-pregnant New Zealand White rabbits. METHODS: On the 24th day of gestation the doe was implanted s.c. with time release pellets containing either glucose (300 mg), sodium butyrate (200 mg) or matching placebo. On the 27th or 30th day maternal (ear vein) and fetal (cardiac puncture) blood samples were drawn for glucose and insulin determinations. Fetal surfactant pools (both intra- and extracellular) were quantitatively harvested using differential and density gradient centrifugation and their phospholipid profiles determined. Data were statistically compared with ANOVA and Duncan's Multiple Range Test. RESULTS: Neither glucose nor sodium butyrate affected maternal plasma glucose or insulin. Both metabolites significantly increased fetal plasma insulin, decreased fetal plasma glucose but did not delay any of the parameters of surfactant maturation examined. CONCLUSIONS: Fetal hyperinsulinemia, whether attained by prolonged exposure to elevated glucose or sodium butyrate in vivo does not appear to be the causative agent for delayed lung maturity which frequently occurs in infants of diabetic mothers.

Animals↗
PubMed2000

Modulation of porcine adipocyte beta-adrenergic receptors by hormones and butyrate.

The beta-adrenergic receptors (betaAR) on the surface of mammalian cells are desensitized when the cell is stimulated by betaAR agonists to eliminate excessive response by the cell. Investigations with adipocytes, primarily rodent-derived cells, indicate other hormones and substrates also can modulate the individual betaAR subtypes. For example, glucocorticoids decrease the beta1AR and the beta3AR but increase the beta2AR. Insulin decreases the beta3AR. Thyroid hormones increase the beta3AR and butyrate increases beta1AR and beta2AR but dramatically decreases beta3AR. Because porcine adipocytes have unique functional and ligand-binding properties compared to rodent adipocytes and because porcine adipocytes contain predominantly beta1AR, compared to rodent adipocytes with predominantly beta3AR, we expect the regulation of porcine adipocyte betaAR by hormones and substrates to be different from that in rodent adipocytes. Isolated porcine adipocytes were incubated for 6 and 21 h without and with dexamethasone, insulin, triiodothyronine, or butyrate. Cells incubated without hormone or butyrate had a decreased betaAR number at 21 h. The beta1AR and beta2AR transcript concentrations were decreased after 6 h and tended to rebound after 21 h of incubation. Dexamethasone did not change the total betaAR number but tended to increase the beta1AR and beta2AR transcript concentrations. Insulin increased the betaAR number and decreased both transcript concentrations at 21 h. Triiodothyronine and butyrate did not change the receptor number or transcript concentrations. The results indicate that betaAR transcript concentrations do not accurately predict the betaAR protein concentration (estimated by ligand binding). Results also indicate that betaAR in porcine adipocytes are relatively unresponsive to hormones and butyrate compared to rodent-derived adipocytes described in the literature.

Adipocytes↗
PubMed2000

Net portal appearance of volatile fatty acids in sheep intraruminally infused with mixtures of acetate, propionate, isobutyrate, butyrate, and valerate.

The net portal appearance of volatile fatty acids (VFA) was investigated in four ruminally fistulated and multicatheterized sheep. During the experiments, the sheep were fed once every hour for 14 h and intraruminally infused with mixtures of VFA for the 12 h commencing 2 h after the initiation of the hourly feeding protocol. Paired arterial and portal blood samples were obtained hourly during the last 6 h of the experiments. In the control treatment (1), only water was infused intraruminally. In Treatments 2 through 4, the intraruminal infusion rates of propionate (40 mmol/h), isobutyrate (5 mmol/h), and valerate (5 mmol/h) were unchanged. In Treatments 2, 3, and 4, the acetate infusion rate was 100, 60, and 20 mmol/h, respectively, and the butyrate infusion rate was 10, 30, and 50 mmol/h, respectively. Thus, the infusion rate of VFA carbon was constant across Treatments 2 through 4. Portal recovery estimated from the increased net portal appearance in Treatments 2 through 4 compared to the control treatment was 85% for propionate and 60% for isobutyrate, and these recoveries were unaffected by treatment. The portal recovery of butyrate increased (from 21 to 32%) with increasing infusion rate of butyrate and decreasing infusion rate of acetate, as did the portal recovery of valerate (from 14 to 31%). The portal recovery of acetate was 55%, when measured as net portal appearance. Thus, it seems that the capacity for beta-oxidation in ruminal epithelium is limited, which would explain the increasing portal recovery of butyrate and valerate with increasing infusion rate of butyrate, when infusion rate of VFA carbon is unchanged.

Acetates↗
PubMed1995

Stimulation of butyrate absorption in the human rectum in vivo.

BACKGROUND: Models of short-chain fatty acid absorption have focused on the stimulation of sodium absorption, an effect mainly located in the proximal colon of man. With the present efforts to utilize butyrate enemas as a treatment of ulcerative colitis, it seemed important to assess the transport in the rectum. METHODS: Non-equilibrium dialysis of the rectum was applied by placing dialysis bags containing various electrolyte solutions in the rectum of volunteers for 30 min. In this period changes in ion concentrations were linear with time. Net absorption and secretion rates were calculated from the change in fluid composition. RESULTS: Sodium absorption was highest (24 +/- 8 mumol/cm2 h) in the presence of chloride and lowest (16 +/- 2 mumol/cm2 h) in the presence of bicarbonate and butyrate. Butyrate (70 mmol/l) was absorbed at a high rate of 7.1 +/- 2.2 mumol/cm2 h, independent on the presence of chloride, and was accompanied by increased bicarbonate secretion. Butyrate absorption increased to 9.6 +/- 1.8 mumol/cm2 h in sodium-free high-potassium media containing bicarbonate. CONCLUSION: The results show that it is possible to increase butyrate uptake by manipulation of the electrolyte composition in the rectal lumen. Maximal uptake occurred with an electrolyte composition that was similar to the natural rectal content. The information gathered could be useful in designing enemas for trial in ulcerative colitis, provided the findings can be confirmed in these patients.

Adult↗
PubMed2000

Potential clinical use of butyric acid derivatives to induce antigen-specific T cell inactivation.

Compounds with the capacity to induce antigen-specific unresponsiveness in CD4(+) T cells can in some clinical situations be more beneficial than general immune suppressants. Newly synthesized ester, ester/amide, and amide derivatives of butyrate with the capacity to induce antigen-specific T cell unresponsiveness in vivo and in vitro were tested here. The ester and ester/amide derivatives of butyrate were shown to block proliferation by interleukin-2-stimulated murine Th1 cells in vitro. A 3-day treatment with these same two derivatives also suppressed a primary antibody response to a thymus-dependent antigen in mice. In addition, even a single injection of the ester derivative of n-butyrate 2-(4-morpholinyl)ethyl butyrate hydrochloride (MEB) on day 2 or 3 after immunization suppressed the generation of memory T cells capable of proliferating to antigen or of promoting a secondary antigen-specific antibody response. MEB also induced antigen-specific unresponsiveness in antigen-activated, but not resting or interleukin-2-activated, T cells in vitro. DNA analysis showed that regardless of when MEB was added to the cultures, it induced the eventual G(1) sequestration of essentially all activated Th1 cells. Because G(1) blockade is associated with Th1 cell anergy, this finding suggests that MEB has the potential to induce anergy in already-activated CD4(+) T cells. Taken together, the results presented here establish MEB as a novel means of inducing anergy in CD4(+) T cells both in vitro and in vivo and underscore the likelihood that MEB and/or other butyrate derivatives can be used as immunotherapeutic reagents.

Animals↗
PubMed2000

Comparisons of the anti-proliferative effects of butyrate and aspirin on human colonic mucosa in vitro.

The short-chain fatty acid butyrate is regarded as a regulative agent in haemostasis of mucosal cell turnover. Inhibition of prostaglandin E2 synthesis is particularly involved in this regulation process. In the present study, proliferation was stimulated in colonic biopsies of 12 healthy subjects (age 51.3 years, range 25-81) by incubation with deoxycholic acid (5 micromol/l DCA). The anti-proliferative and cyclo-oxygenase-inhibiting properties of butyrate (10 mmol/l BUT) and of aspirin (555 micromol/l ASA) were investigated. Colonic cell proliferation was determined by bromodeoxyuridine immunohistochemistry. PGE2 release into the incubation medium was measured by radioimmunoassay. Incubation with DCA/ASA, DCA/BUT and DCA/ASA/BUT revealed a significant reduction in crypt cell proliferation as measured by the labelling index of the whole crypt in comparison to incubation with DCA alone (DCA/ASA: 0.14, P < 0.01; DCA/BUT: 0.15, P < 0.05; DCA/ASA/BUT: 0.15, P < 0.05, versus DCA: 0.18). The labelling index for the upper 40% of the crypt was only lower after incubation with DCA/ASA (0.023) compared to DCA (0.028) (P < 0.05). PGE2 release from biopsy specimens was only significantly decreased in the incubation media where ASA was added (DCA/ASA: 29.0 pg/mg mucosa/h, P < 0.005; DCA/ASA/BUT: 31.4 pg/mg mucosa/h, P < 0.01 versus DCA: 56.9 pg/mg mucosa/h). Butyrate and aspirin showed no synergistic effects. The results indicate a normalization of DCA-induced hyperproliferation of colonic mucosa by butyrate, and, even more efficiently, by aspirin. The data support the hypothesis that butyrate and aspirin can act as chemopreventive agents in colon carcinogenesis.

Adult↗
PubMedDate not supplied

Tributyrin, a butyrate precursor, impairs growth and induces apoptosis and differentiation in pancreatic cancer cells.

BACKGROUND: The aim of this study was to investigate whether tributyrin, a natural butyrate pro-drug, as well as butyrate itself could affect growth, differentiation and apoptosis in two human pancreatic cancer cell lines in culture. MATERIALS AND METHODS: Proliferation was studied by cell counting using crystal violet staining. Cell differentiation was assessed by measuring the alkaline phosphatase activity and cell death by DAPI nuclear staining. RESULTS: In MiaPaca-2 cells both tributyrin and butyrate reduced growth, with IC50 values of 1.1+/-0.2 mmol/ and 3.6+/-0.7 mmol/L respectively. Both 1 mmol/L tributyrin and 3 mmol/L butyrate induced a similar degree of apoptosis in MiaPaca-2 and Capan-l cells and stimulated differentiation in Capan-l cells equally. CONCLUSION: Our data may provide a rationale for the therapeutic use of peroral tributyrin in patients with pancreatic cancer, because this drug enables plasma concentrations of butyrate which inhibit growth, induce differentiation and cause apoptosis in pancreatic cancer cells.

Apoptosis↗
PubMedDate not supplied

Butyrate-enhanced TNFalpha-induced apoptosis is associated with inhibition of NF-kappaB.

BACKGROUND: Tumor necrosis factor (TNFalpha)-induced apoptosis is limited by concomitant activation of nuclear factor kappa B (NF-kappaB)-dependent anti-apoptotic genes. Butyrate inhibits NF-kappaB activation so that co-treatment with butyrate effectively enhances TNFalpha-induced apoptosis. In this context, the inhibition of NF-kappaB activation and subsequent modulation of (NF-kappaB)-dependent genes was assessed MATERIALS AND METHODS: Human colon adenocarcinoma cells (SW620) were incubated with TNFalpha and butyrate. Apoptosis was determined by annexin V/propidium iodide staining and flow cytometry. NF-kappaB activation was detected by electrophoretic mobility shift assay. The expression of NF-kappaB-dependent genes was assessed by RNase protection assay (RPA) RESULTS: The TNFalpha/butyrate combination yielded an additive increase in the number of apoptotic cells. NF-kappaB nuclear translocation was successfully inhibited by co-incubation with butyrate. However, the expression pattern of NF-kappaB-dependent genes remained essentially unchanged CONCLUSION: Butyrate enhances TNFalpha-induced apoptosis in the human adenocarcinoma cell line SW620. This additive effect may, at least in part, be mediated by the inhibition of NF-kappaB activation, presumably by impairing the anti-apoptotic properties of NF-kappaB.

Adenocarcinoma↗
PubMed2002

[Molecular mechanism of inhibition of sodium butyrate on activation of tumor associated aromatase promoters].

BACKGROUND & OBJECTIVE: Sodium butyrate, a histone deacetylase inhibitor, can inhibit tumor conditioned medium-induced levels of promoter II and I. 3-specific transcripts. This study was designed to investigate the action of sodium butyrate on promoter II and I. 3 activity, which can be directed to elucidation of local estrogen production in breast cancer. METHODS: Primary human adipose fibroblasts (HAF) treated with MCF-7 breast cancer cell-conditioned medium were used as a cell model system. Promoter II and I. 3 deletion luciferase constructs was transfected into HAF. Western blotting and electrophoretic mobility shift assay were performed to evaluate the effect of sodium butyrate on promoter II and I .3. RESULTS: Breast cancer cell-conditioned medium enhanced phosphorylation of activator transcription factor-2 (ATF-2) which was the main modulatory subtype in CREB/ATF-2 family. The effect of sodium butyrate on aromatase expression in breast tumor fibroblasts was mediated by inhibition of phosphorylation of ATF-2, and hence, the inhibition of binding of a transcriptional complex containing phosphorylated ATF-2, C/EBP beta and CREB binding protein (CBP) to promoter II/I. 3 regulatory region. CONCLUSIONS: Sodium butyrate reduces the level of aromatase mRNA arising from cancer-induced promoter region. The aberrant activation of promoter II and I. 3 in HAF is dependent on the phosphorylation of ATF-2.

Activating Transcription Factor 1↗
PubMed2000

[Differentiation of human glioma cells BT-325 induced by sodium butyrate].

OBJECTIVE: To study the differentiation of human glioma cells BT-325 induced by sodium butyrate in vitro. METHODS: BT-325 cells were treated with 1 mmol/L sodium butyrate. Flow cytometry was used to analyze the cell cycle. Cell differentiation was identified by flow cytometry and Western blot analysis. RESULTS: After 6-8 days of sodium butyrate treatment, the differentiation characters could be observed distinctively, such as the reduced cell density, the increased cell size and the marked increase in cell process formation and cell-to-cell connection. At the same time, Western blot showed that the amount of glial fibrillary acidic protein was elevated after the sodium butyrate treatment. CONCLUSION: Human glioma cells BT-325 could be induced to differentiation by sodium butyrate.

Brain Neoplasms↗
PubMed2004

Down-regulation of matrix-invasive potential of human liver cancer cells by type I interferon and a histone deacetylase inhibitor sodium butyrate.

We have demonstrated anti-proliferation and anti-metastasis effects of both interferon-alpha and a histone deacetylase inhibitor, sodium butyrate, on human liver cancer cell lines. In this study, invasive ability of human liver cancer cell lines through the matrix-coated membrane was examined and inhibitory effect of interferon-alpha and sodium butyrate was investigated. Among six human liver cancer cell lines, HLE and HLF showed high invasive ability using the Matrigel invasion assay. This invasion ability was significantly inhibited by pretreatment of the cells with 1000 IU/ml of interferon-alpha or 2 mM of sodium butyrate. Gelatin zymography and the matrix metalloproteinase-2 and -9 activity assay showed that these two cell lines produce active- and pro-matrix metalloproteinase-2 and -9, and their activity was significantly reduced by pretreatment with both agents. Real-time quantitative reverse transcription-polymerase chain reaction showed decrease in matrix metalloproteinase-1 mRNA levels by pretreatment with both agents, but mRNA levels of tissue inhibitor of matrix metalloproteinase-1 and -2 were differently modulated by interferon-alpha and sodium butyrate. These results suggest that interferon-alpha and sodium butyrate reduce a chance of invasion and metastasis of human liver cancer cells by inhibiting matrix metalloproteinase activity, although its inhibitor is differently regulated.

Antineoplastic Agents↗
PubMed2004

[Sodium butyrate induces rat hepatic oval cells differentiating into mature hepatocytes in vitro].

OBJECTIVE: To elucidate the effects of sodium butyrate on rat hepatic oval cell differentiation in vitro. METHODS: Hepatic oval cells were isolated from rats fed with a choline-deficient diet supplemented with 0.1% (w/w) ethonine for 4 to 6 weeks. The cultured hepatic oval cells were identified by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). After hepatic oval cells were treated with sodium butyrate, the morphological changes were studied through Giemsa staining and the albumin expression level was tested by Western blot. RESULTS: Immunohistochemical results showed the isolated cells were positive for both mature hepatocyte marker albumin and bile duct cell marker cytokeratin-19. Furthermore, RT-PCR results showed that the cells expressed stem cell marker c-kit, but not hematopoietic stem cell marker CD34. In short, the isolated cells were rat hepatic oval cells. 0.75 mmol/L sodium butyrate induced obvious phenotype changes of hepatic oval cells, including enlargement of the oval cells, a decrease in nucleus to cytoplasm ratio, and a 50% increase in the number of binucleated cells. Western blot results showed that 0.75 mmol/L sodium butyrate markedly raised the expression of albumin. CONCLUSION: Sodium butyrate, a differentiation promoting agent, can induce rat hepatic oval cells (liver progenitor cells) to differentiate into mature hepatocytes in vitro.

Animals↗
PubMed2005

Response of HT115, a highly invasive human colorectal adenocarcinoma cell line, to sodium butyrate treatment and glucose deprivation.

Sodium butyrate or glucose deprivation induce a more differentiated phenotype in many cancer cells. The aim of this study was to determine whether the induction effect of butyrate and/or glucose deprivation is dependent, in some way, on the differentiation state of individual cell lines. Sodium butyrate enhanced alkaline phosphatase activity and induced formation of an ultrastructurally more differentiated phenotype in both HT29 and HT115 cell lines. Interestingly, the more invasive HT115 cells responded more strongly to butyrate treatment. On the other hand, the differentiation effect of glucose deprivation was much less prominent in the HT115 cell line in comparison with HT29 cells. Our data confirm the influence of the malignant potential of the cells on their response to treatment with differentiation and apoptosis-inducing agents. Butyrate treatment also enhanced the adhesiveness of HT115 cells. Since E-cadherin was not found in these cells, while the level of CEACAM1 was increased, it is obvious that the CEACAM1 molecules are involved in HT115 cell-cell adhesion.

Adenocarcinoma↗