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PubMed1985

The 25 kDa protein kinase inhibitor present in liver cell is absent in fast growing HTC cells and is induced in sodium butyrate treated cells.

We have recently characterized a cAMP independent protein kinase inhibitor in rat liver. This inhibitor is absent or inactive in fast growing HTC cells and is induced according to exponential kinetics by sodium butyrate, a compound which arrests cell growth at the G1 phase of the cell cycle. It is suggested that the inhibitor could be involved in cell growth regulation.

Animals↗
PubMed1989

Sodium-n-butyrate induces secretion and substrate accumulation of p52 in Kirsten sarcoma virus-transformed rat kidney fibroblasts.

1. A group of five transformation-responsive secreted proteins, ranging in molecular mass from 31 to 70 kDa, were identified in cultured normal rat kidney (NRK) fibroblasts. 2. One such protein (p52) was found to be a major secreted and substrate-attached component of NRK cells. 3. Kirsten sarcoma virus-transformed NRK cells failed to accumulate p52 in either the secreted or substrate-associated protein compartments; this protein was inducible, however, in transformed cells by culture in 2 mM sodium-n-butyrate. 4. Kinetics of p52 induction in transformed NRK cells, relative to the time course of increased cell spreading, and its enrichment in the substrate-associated protein fraction suggest that p52 might function in cell-substrate attachment.

Animals↗
PubMed1989

Cytoarchitecture of ras oncogene-expressing tumor cells: butyrate modulation of substrate adhesion, cytoskeletal actin content and subcellular microfilament distribution.

1. The subcellular distribution of particular cytoskeletal (CSK) and cell-substrate adhesive elements was assessed during the morphologic response of cultured tumor cells to the shape modulating agent sodium butyrate (NaB). 2. NaB induced marked increases in cellular and CSK actin content and in the matrix-associated proteins fibronectin and p52. 3. Subcellular fractionation indicated disproportionate increases in the actin content of the substrate-attached cellular residue (SAM fraction) which contains the majority of cell-substrate adhesive elements. 4. Augmented cell spreading and substrate attachment characteristic of NaB-treated cells is likely due to increased elaboration of cell-to-substrate adhesive structures and reflected in an enhanced deposition of actin into the CSK and SAM compartments.

Actin Cytoskeleton↗
PubMed1994

Modulatory effect of sodium butyrate on AluI-induced chromosomal aberrations in CHO cells.

Exponentially growing CHO cells exposed to millimolar concentrations of sodium butyrate (SB) for 24 h were treated with AluI using two methods of cell poration, i.e., electroporation and streptolysin O (SLO). Under both conditions, SB was found to induce a 2-4-fold increase in AluI-induced chromosomal aberrations. When cells in monolayer were treated with AluI/SLO, lower concentrations of SB (2.5 mM) and AluI (1-4 U/ml) were required to produce a similar effect as that observed for electroporated cells, demonstrating the differential sensitivity of the two methods. Furthermore, in AluI/SLO-treated cells, a higher percentage of cells was found to show increased frequencies of aberrations per cell, compared to AluI/electroporated cells. The mechanism by which SB modulates the cell response to AluI treatment might involve changes in chromatin configuration thereby increasing the accessibility of AluI to different parts of chromatin.

Animals↗
PubMed1991

Sodium butyrate-inducible replication of human cytomegalovirus in a human epithelial cell line.

Replication of human cytomegalovirus (HCMV) in a human epithelial thyroid papillary carcinoma cell line (TPC-1) was restricted. However, pretreatment of these cells with 5 mM sodium butyrate (NaB) for 24 hr before infection enhanced both HCMV yield and infectious center titer to a similar level of that seen in human embryonic lung fibroblast cells. Immunofluorescence staining, gel electrophoresis, and Northern blot analysis revealed that TPC-1 cells are nonpermissive for expression of HCMV major immediate early (IE1) functions, but many of the cells become permissive after being treated with NaB. The presence of cycloheximide during NaB pretreatment of the cells efficiently diminished the stimulatory effect of NaB on expression of the IE1 gene. Therefore, it appeared that NaB induces the synthesis of a cellular protein(s) which apparently plays an important role in the conversion of nonpermissive cells to a permissive state for expression of this critical viral gene. Transient chloramphenicol acetyltransferase (CAT) assay experiments indicated that in TPC-1 cells the HCMV-CAT construct which contains the complete IE1 promoter regulatory region was expressed poorly, whereas a high level of CAT activity was detectable in the NaB-treated cells. Therefore, these results suggest that the enhancing effect of NaB on HCMV replication is expressed through some host cellular factor(s), and the HCMV IE1 promoter regulatory region is most likely to be the primary target of NaB action.

Antibodies, Monoclonal↗
PubMed1984

Sodium butyrate affects the cytotoxic and mutagenic response of V79 Chinese hamster cells to the genotoxic agents, daunorubicin and U.V. radiation.

It has been suggested that conditions which lead to modifications in the chromatin structure could be responsible for an increased accessibility of DNA to genotoxic agents in eukaryotic cells. With this in mind, the cytotoxic and mutagenic activity of the anthracycline antibiotic, daunorubicin, and of UV radiation was assayed on V79 Chinese hamster cells pretreated or not with 5 mM sodium butyrate, an agent known to induce modifications in the chromatin structure: this treatment in fact proved to induce the hyperacetylation of the core histones, and moreover to enhance the cytotoxic response of the cells to both daunorubicin and UV radiation and the mutagenic response to daunorubicin.

Animals↗
PubMed1986

Induction of differentiation in Friend erythroleukemia cells with dimethyl sulfoxide, hexamethylene bisacetamide and sodium butyrate is not accompanied by changes in proviral DNA or its expression.

The integration pattern, copy number and DNA expression of the Friend virus genome was examined in Friend erythroleukemia cells induced to differentiate with dimethyl sulfoxide, hexamethylene bisacetamide and sodium butyrate. The integrated proviral DNA in Friend erythroleukemia cells was examined by Southern hybridization with a cloned Friend virus (F-MuLV) probe at days 1 and 4 following inducer treatment, as well as on day 6 at which time the cells had remained for 48 h in inducer free medium. KpnI fragments 9 and 5.7 kb long were observed. The copy number of each fragment remained constant throughout the erythroid differentiation process. EcoRI digestion of DNA isolated from cells at different times following the inducer treatment demonstrated multiple integration sites of the proviral genome, which also remained constant during the differentiation process. Proviral DNA expression was examined at 4 h and 4 days following inducer treatment as well as on day 6 by which time cells remained for 48 h in inducer free medium. Northern blot hybridization to the F-MuLV probe indicated no change in the provirus gene expression independent of the class of inducers. These observations reinforce our conclusions that the viral genome and its transcription product do not play a major role in the differentiation process of Friend erythroleukemic cells.

Acetamides↗
PubMed1985

Induction of the expression of HLA class I antigens on K562 by interferons and sodium butyrate.

Using sodium butyrate and alpha, beta, and gamma interferons as inducing agents it has been possible to demonstrate the triggering of HLA class I antigen synthesis in the K562 cell line. This cell line, widely used to study hemopoietic differentiation, does not naturally express HLA antigens. This effect was confirmed by the detection of HLA class I antigens on the cell membrane with specific monoclonal antibodies, by immuneprecipitation, and by isolation of specific HLA ABC messenger RNA, in the induced cells. No synthesis of HLA class II antigens was observed. Because leukemic cells can be considered as a model representing certain stages of normal hemopoietic differentiation, the expression of HLA antigens on K562 cells induced to differentiate could be interpreted as an event related to the process of differentiation itself. The lack of expression of DR antigens may result from a genetic defect as observed for beta 2-microglobin in Daudi cells.

Antibodies, Monoclonal↗
PubMed1986

CD 1-8 antigens on human diphtheria toxoid T lymphocyte clones: expression and modulation by TPA, sodium butyrate, and 5-azacytidine.

The modulation of antigen expression on the surface of TLC by different differentiation inducers as well as the inhibition of the TLC proliferative response by specific MoAbs may lead to a clarification of the role of various surface molecules studied in antigen-specific T-cell response. We investigated the expression of CD 1-8 antigens on the surface of diphtheria toxoid or varidase specific TLC with a series of MoAb. CD1 and CD8 antigens were not expressed on the proliferative TLC. CD2, CD3, CD4, and CD5 antigens were homogeneously expressed on all TLC in contrast to CD6 and CD7 antigens which were present on only a fraction of the cells in a given TLC. In functional assays, anti-CD2, anti-DR VI-15C, and anti-CD25 MoAbs blocked the proliferative response to DT and anti-CD3, anti-CD4, anti-D44 MoAbs had intermediate inhibition effects. Anti-CD5, anti-CD6, and anti-CD7 MoAbs did not inhibit the proliferative response. Surface marker analysis revealed that the expression of CD2 to CD7 antigens (and also CD25) may be modified following incubation of the TLC with TPA or sodium butyrate but not with 5-azacytidine. TPA greatly decreased the expression of CD3 and CD4 antigens after a 6-hr exposure. Preincubation of TLC cells with TPA inhibited the mitogenic effect of anti-CD3 MoAbs on TLC cells in proliferative assays, but did not inhibit their capacity to proliferate in response to DT despite low levels of CD3 and CD4.

Antibodies, Monoclonal↗
PubMed1984

Effect of dimethylsulfoxide and butyrate on 5'-nucleotidase of human renal carcinoma cells.

The effect of dimethylsulfoxide (DMSO) and butyrate, agents which induce differentiation of certain cancer cells, on membrane associated 5'-nucleotidase (5'-NT) of 2 human renal carcinoma cell lines (Cur and Caki) was investigated. Under a variety of conditions of agent addition, 5'-NT specific activity increased in Cur and decreased in Caki cells. This opposite response pattern was observed for assays performed on lysates at pH 9.0 and 7.4 and assays with intact cell monolayers, even under conditions of identical cellular growth inhibition. It is concluded that the cell lines responded in a fundamentally different way to the chemical agents. An increase in 5'-NT has correlated with cell maturation for a number of processes. The DMSO induced increase in Cur 5'-NT was dependent on protein synthesis.

5'-Nucleotidase↗
PubMed1992

Sodium butyrate alters the response of a human colon carcinoma cell line to transforming growth factor-beta 1.

The effects of sodium butyrate (NaB) on the response of the RCA human colon carcinoma cell line to transforming growth factor-beta 1 (TGF-beta 1) were examined. NaB induced differentiation, as judged by an increase in cellular alkaline phosphatase, in the RCA cells and this differentiation was accompanied by a decreased growth rate. TGF-beta 1 did not significantly alter the growth or state of differentiation of the RCA cells. The growth rate of cells treated simultaneously with NaB and TGF-beta 1 was similar to that of control untreated cells while the alkaline phosphatase levels remained comparable to cells treated with NaB. Addition of TGF-beta 1 to cells grown in the presence of NaB resulted in a stimulation of growth. Cells pretreated with TGF-beta 1 remained sensitive to the growth inhibitory and differentiation inducing effects of NaB. These results suggest that NaB may alter the expression of proteins responsible for a stimulatory signal response to TGF-beta 1 in RCA cells.

Alkaline Phosphatase↗
PubMed1986

Contrasting effects of the differentiating agent sodium butyrate on recovery processes after x-irradiation in heterogeneous human colon tumor cells.

The X ray survival responses of two clonal subpopulations of cells (clones A and D) from a heterogeneous human colon adenocarcinoma (DLD-l) were studied in unfed plateau phase cultures either as control cultures or in cultures grown for three passages in medium containing the differentiating agent sodium butyrate (NaB, 2 mM). Specifically, the cultures were studied with regard to their ability to express both potentially lethal and sublethal damage recovery (PLDR and SLDR). Growth in NaB-containing medium enhanced the radiation sensitivity of both cell lines in the low dose ("shoulder") region of the survival curve. For clone A, the Dq value was reduced by 59%, and for clone D, the Dq value was reduced by 96%. NaB treatment increased both the rate and the extent of PLDR in both cell lines as assessed by single dose kinetic studies. However, when split dose experiments are performed to assess the expression of SLDR, NaB pretreatment was shown to totally inhibit the expression of SLDR, and also to alter the expression of PLDR under these conditions. These data suggest that PLDR and SLDR are separate, yet related, cellular recovery processes. In addition, NaB may be useful as an adjunct to radiotherapy by virtue of its ability to sensitize tumor cells in the dose range conventionally used for therapy, as well as by inhibition of sublethal damage recovery.

Adenocarcinoma↗
PubMed1987

Effects of nucleoside analogs and sodium butyrate on recovery from potentially lethal X ray damage in human colon tumor cells.

The effects of 5-azacytidine (5-aza-CR) and 5-aza-2'-deoxycytidine (5-aza-CdR) both alone and in combination with sodium butyrate (NaB) on intrinsic radiation sensitivity and ability to recover from potentially lethal damage (PLDR) were studied in two subpopulations of cells (clones A and D) from a heterogeneous human colon adenocarcinoma (DLD-1). Growth for three passages in medium containing 1 mM NaB alone enhanced radiation cell killing in the low dose ("shoulder") region of the survival curve for both cell lines. Neither 1.0 microM 5-aza-CR nor 0.25 microM 5-aza-CdR alone enhanced cell killing. However, treatment of these cells with a combination of either 5-aza-CR or 5-aza-CdR and NaB enhanced radiation cell killing at a clinically relevant dose level of 2.0 Gy by approximately 25% for both clone A and clone D cells. Also, while exposure to these differentiation-inducing agents separately enhanced the expression of PLDR in both tumor subpopulations, treatment with either of the combinations reversed this increase in PLDR. These results indicate that the gene-activating agents 5-aza-CR, 5-aza-CdR, and NaB may interact to modify the radiation sensitivity of two human tumor cell lines. Such combinations may prove useful clinically, if enhanced X ray cell killing of tumor cells can be achieved without a concomitant enhancement of recovery from potentially lethal X ray damage.

Adenocarcinoma↗
PubMed1988

Potentiation of X ray sensitivity by combinations of sodium butyrate and buthionine sulfoximine.

The ability of various concentrations of the differentiation-inducing agent sodium butyrate (NAB, 0-2 mM) to produce radiosensitization in human colon tumor cells when combined with varying concentrations of the irreversible inhibitor of gamma-glutamyl cysteine synthetase, buthionine sulfoximine (BSO, 0-0.75 mM) was studied. We have previously shown that high concentrations of each agent in combination (2 mM NAB + 0.5 mM BSO) produced a supra-additive effect in terms of radiosensitization as indicated by a decrease in the quasi-threshold value (Dq) of the single dose survival curve; we wished to define responses at other concentrations. Cells were adapted in vitro to growth in medium containing NAB for 3 passages prior to x-irradiation and BSO was given acutely 24 hrs before the x-irradiations. The most effective combination was 0.3 mM NAB + 0.75 mM BSO. These data suggest that adaptation of tumor cells to chronic low levels of a differentiation-inducing agent such as NAB followed by administration of BSO just prior to irradiation might be an effective combination in producing increased response of solid tumors.

Buthionine Sulfoximine↗
PubMed1991

Isobutyrate as a precursor of n-butyrate in the biosynthesis of tylosine and fatty acids.

Labelled sodium isobutyrate [(CD3)2-CHCOONa] was added to the culture medium of Streptomyces fradiae and up to 14 atoms of deuterium were found to be incorporated into a molecule of tylosin aglycone (tylactone). This observation is in accordance with the data in the literature. When fatty acids were analyzed, as much as 34% of the isobutyrate incorporated into the cell was formed to be transformed into butyrate that was used for the synthesis of even, straight-chain fatty acids; 57% of the labelled isobutyrate was incorporated into the even isoacids, whereas 9% was degraded to propionate and further used for the synthesis of the odd acids.

Butyrates↗
PubMed1986

Enhancement of cadmium-induced metallothionein synthesis in cultured TRL 1215 cells by butyric acid pretreatment.

Cultured TRL 1215 cells in log phase of growth were exposed first to butyric acid (BA; 0.1-2.0 mM) and then 48 h later, to cadmium (Cd; 10 microM). Metallothionein (MT) concentrations were measured 24 h after Cd addition. Cd alone caused approx. a 10-fold increase in cellular MT levels, while BA alone had no effect. BA pretreatment followed by Cd exposure, however, resulted in MT levels up to 25 times those in control cells. Concurrent exposure to hydroxyurea (HU) eliminated the enhancing effect of BA pretreatment on induction of MT by Cd, indicating that DNA synthesis is required. BA-pretreated cells did not show marked increases in cellular uptake of Cd. BA pretreatment enhances Cd induction of MT synthesis through a mechanism that is dependent on the synthesis of DNA.

Animals↗
PubMed1992

Sodium butyrate stimulates polyamine biosynthesis in colon cancer cells.

Differentiation inducers act through polyamine-dependent and independent pathways. Sodium butyrate (NaB) inhibits proliferation and induces terminal differentiation in human and murine cancer cell lines. An effect of this agent on polyamine biosynthesis has not been demonstrated previously. In the present study, we examined the effects of NaB on polyamine biosynthesis in mouse colon cancer (MC-26) cells. All studies were performed on exponentially growing cells, and ODC and polyamine transport measurements were performed as described previously. NaB inhibited the growth of MC-26 cells in a dose-dependent manner. Cell shape was significantly altered by treatment with NaB (development of dendritic-like processes and flattening and spreading out of cells on culture dishes). NaB stimulated ODC activity in a dose-dependent manner. The activity was elevated by 8 h after treatment, and at 48 h there was a ten-fold increase in activity (compared with control activity). The increase in ODC activity led to an increase in polyamine biosynthesis; putrescine, spermidine, and spermine levels in MC-26 cells were significantly elevated by 24 h after treatment with NaB. Polyamine uptake was similar in control cells and cells treated with NaB alone. Our finding of significant stimulation of polyamine uptake by NaB after inhibition of endogenous synthesis (by an ODC-dependent pathway) in DFMO-treated cells suggests that cellular requirements are increased for polyamines in NaB-treated cells. We conclude that polyamine-dependent processes are important in the mechanism of action of NaB in colon cancer cells.

Animals↗
PubMed1997

Interleukin-2-dependent augmentation of the anti-TNP antibody production by sodium butyrate in cultured murine splenic B cells.

Previously we found that sodium butyrate (NaBu) markedly enhanced production of the antibody specific for a T-cell-dependent antigen, sheep red blood cells (SRBC) in murine splenocytes (Kishiro, Y., Ueda, K., Fujiwara, M. and Yamamoto, I., Jpn J. Phamacol., 1994 66, 369-376. To gain a better understanding of the target cells for NaBu's action on antibody responses, we have utilized the T-cell-independent antigen, trinitrophenyl-lypopolysaccharide (TNP-LPS) as a stimulant and have examined an effect of NaBu on the anti-TNP antibody production in vitro. NaBu markedly increased the anti-TNP plaque-forming cell (PFC) responses in murine whole splenocytes, but not in murine splenic B cells. Addition of T-cells or the concanavalin A supernatant (CAS) from murine splenocytes to the B cell cultures completely restored the enhancing effect of NaBu. This effect of CAS was totally blocked by an anti-interleukin (IL)-2 antibody and partially by an anti-IL-1 beta or anti-IL-4 antibody. The full enhancing effect of NaBu was also detected when IL-2 was added to the B cell cultures, while IL-2 alone had no stimulatory effect on the control PFC response. IL-1 beta alone significantly stimulated the antibody production and adding NaBu to this IL-1 beta-supplemented culture caused a further increase. Neither IL-4 alone nor NaBu plus IL-4 had any effect on the PFC response. NaBu did not affect the expression of the IL-2 receptor alpha- and beta-chains in B cells stimulated with TNP-LPS. These results suggest that NaBu is an agent that promotes B cell differentiation in vitro in an IL-2-dependent manner.

Animals↗