Butyric acid, a potent inducer of erythroid differentiation in cultured erythroleukemic cells

Leder, Aya; Leder, Philip

doi:10.1016/0092-8674(75)90107-5

Cited by 643 publications

(228 citation statements)

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“…The short-chain fatty acid sodium butyrate (NaBt), a natural fermentation product of dietary fibre (Cummings, 1981) has been found to induce differentiation in a number of different cell types including colonic cells (Leder and Leder, 1975;Prasad and Sinha, 1976). Furthermore, it has previously been established that NaBt can induce differentiation in colorectal cell lines, and this induction of differentiation is evidenced by increased expression of the differentiation markers alkaline phosphatase (ALP) and E-cadherin (Butt et al, 1997).…”

Section: Treatment With the Differentiation Agent Sodium Butyrate Resmentioning

confidence: 99%

Transcriptional down-regulation of the retinoblastoma protein is associated with differentiation and apoptosis in human colorectal epithelial cells

et al. 2001

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SummaryThe aim of this study was to investigate the regulation of Rb protein expression in relation to increased differentiation and induction of apoptosis in colonic epithelial cells. In vivo, Rb protein expression was found to be down-regulated towards the top of the normal colonic crypt, coincident with the region of differentiation and apoptosis, but highly expressed in colonic carcinoma tissue. Using in vitro models to study the regulation of Rb expression in pre-malignant colonic epithelial cells, we have been able to show for the first time that Rb protein expression is transcriptionally down-regulated in differentiated pre-malignant cells (in post-confluent cultures) but not in malignant colorectal epithelial cells. Furthermore, suppression of rb protein function by the HPV-E7 viral oncoprotein increased both spontaneous and DNA damage-induced apoptosis. These results suggest that Rb is able to act as a survival factor in colonic epithelial cells by suppressing apoptosis, and that over-expression of pRb in colorectal tumour cells can cause a loss of sensitivity to apoptotic signalling, resulting in aberrant cell survival and resistance to therapy. targeted inactivation of the RB-1 gene in mouse embryonic fibroblasts induces apoptosis. Therefore, pRb appears to suppress apoptosis in some cell systems, perhaps through the sequestration of the E2F-1 protein, which can induce apoptosis if over-expressed (Qin et al, 1994;Field et al, 1996). In this case, pRb needs to be removed or inactivated before apoptosis can occur. To support this, a 30 kD protein has been detected in apoptotic cells harvested from colon tumour cell lines, CMSV40 fibroblasts and BJA-B lymphocyte cells, suggesting that the Rb protein is cleaved during the apoptotic process (Browne et al, 1994;An and Dou, 1996). Furthermore, cleavage at the C-terminus of pRb results in a p100 and ~5 kDa polypeptide (Chen et al, 1997). The p100 Rb protein can still bind to E2F-1 and inhibit E2F-mediated transcriptional activity, but its anti-apoptotic function is reduced, perhaps through its inability to bind to the oncogene MDM2. Thus the growthsuppressive and anti-apoptotic functions of pRb appear to be distinct from one another. The notion that pRb functions can be separated from one another has been explored previously, and experimental evidence indicates that the multiple functions of pRb can be genetically uncoupled, providing distinct functions in cellcycle control or in tissue-specific gene expression during differentiation (reviewed in Yee et al, 1998). Mice with mutations of the N-terminal region of Rb protein exhibit defects in muscle differentiation, whilst retaining the ability to bind to E2F (Riley et al, 1997). Conversely, cells with pRb mutations in the pocket domain are able to differentiate normally even when E2F binding is abrogated (Sellers et al, 1998).The functional loss of the Rb protein, by deletion or mutation, has been implicated not only in retinoblastoma, but in many types of tumour, including bladder, breast, lung and ovarian ca...

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Section: Treatment With the Differentiation Agent Sodium Butyrate Resmentioning

confidence: 99%

Transcriptional down-regulation of the retinoblastoma protein is associated with differentiation and apoptosis in human colorectal epithelial cells

et al. 2001

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“…Murine erythroleukaemia cells infected with the Friend virus (FLC) differentiate in vitro from a proerythroblast-like to a normoblast-like stage producing haemoglobin when they are treated with dimethylsulfoxide (DMSO) or other inducers (Friend et al, 1971;Leder & Leder, 1975;Reuben et al, 1976;Ebert et al, 1976). Chemically induced differentiation is promptly and spontaneously reversed when the inducing agents are removed from the culture medium (Friend et al, 1971).…”

mentioning

confidence: 99%

Inhibition of Friend erythroleukaemia-cell tumours in vivo by a synthetic analogue of prostaglandin E2

Santoro¹,

Jaffe²

1979

Br J Cancer

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Summary.-The effect of 16,16-dimethyl-PGE2-methyl ester (di-M-PGE2), a longacting synthetic analogue of prostaglandin E2, on the replication of Friend erythroleukaemia cells (FLC) in vivo has been studied. Pre-treatment in vitro of both undifferentiated and differentiated FLC with di-M-PGE2 (1 jug/ml) did not alter rates of tumour appearance or growth, but increased the median survival of DBA/2J mice.Systemic administration of di-M-PGE2 (10 1kg/mouse/day) was not toxic to the mice, but significantly inhibited tumour growth and increased median survival in mice injected s.c. with undifferentiated FLC. These effects of di-M-PGE2 were much more pronounced in mice receiving differentiated (DMSO -treated) FLC. In this latter group, the appearance of tumour was also significantly delayed by di-M-PGE2. The different effects of di-M-PGE2 treatment on tumours derived from undifferentiated and differentiated cells suggest that the analogue is acting directly on tumour-cell replication rather than on factors related to the host response.

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“…The active component of NaB is a short‐chain fatty acid (butyric acid), which is a gastrointestinal nutrient. Previous reports have demonstrated that NaB acts as an energy source for cellular differentiation and provides energy for the recovery of damaged cells 4, 5. NaB not only participates in the metabolism of fat and the production of ketone bodies but also in carbohydrate metabolism.…”

Section: Introductionmentioning

confidence: 99%

PLGA‐PNIPAM Microspheres Loaded with the Gastrointestinal Nutrient NaB Ameliorate Cardiac Dysfunction by Activating Sirt3 in Acute Myocardial Infarction

Cheng

Zeng

et al. 2016

Advanced Science

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Acute myocardial infarction (AMI) is the death of cardiomyocytes caused by a lack of energy due to ischemia. Nutrients supplied by the blood are the main source of cellular energy for cardiomyocytes. Sodium butyrate (NaB), a gastrointestinal nutrient, is a short‐chain fatty acid (butyric acid) that may act as an energy source in AMI therapy. Poly(lactic‐co‐glycolic acid)‐Poly (N‐isopropylacrylamide) microspheres loaded with NaB (PP‐N) are synthesized to prolong the release of NaB and are injected into ischemic zones in a Sprague–Dawley rat AMI model. Here, this study shows that PP‐N can significantly ameliorate cardiac dysfunction in AMI, and NaB can specially bind to Sirt3 structure, activating its deacetylation ability and inhibiting the generation of reactive oxygen species, autophagy, and angiogenesis promotion. The results indicate that NaB, acting as a nutrient, can protect cardiomyocytes in AMI. These results suggest that the gastrointestinal nutrient NaB may be a new therapy for AMI treatment, and PP‐N may be the ideal therapeutic regimen.

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Butyric acid, a potent inducer of erythroid differentiation in cultured erythroleukemic cells

Cited by 643 publications

References 4 publications

Transcriptional down-regulation of the retinoblastoma protein is associated with differentiation and apoptosis in human colorectal epithelial cells

Transcriptional down-regulation of the retinoblastoma protein is associated with differentiation and apoptosis in human colorectal epithelial cells

Inhibition of Friend erythroleukaemia-cell tumours in vivo by a synthetic analogue of prostaglandin E2

PLGA‐PNIPAM Microspheres Loaded with the Gastrointestinal Nutrient NaB Ameliorate Cardiac Dysfunction by Activating Sirt3 in Acute Myocardial Infarction

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