Sodium butyrate/retinoic acid costimulation induces apoptosis-independent growth arrest and cell differentiation in normal and ras-transformed seminal vesicle epithelial cells unresponsive to retinoic acid

Buommino, Elisabetta; Pasquali, Daniela; Aa, Sinisi; Bellastella, Antonio; Morelli, Francesco; Metafora, Salvatore

doi:10.1677/jme.0.0240083

Cited by 16 publications

(8 citation statements)

References 48 publications

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“…1998; Tucholski et al . 2001) or rat epithelial SVC1 (Buommino et al . 2000) cells does not induce apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…1997), differentiation (Aeschlimann et al . 1993; Buommino et al . 2000), wound healing (Haroon et al .…”

mentioning

confidence: 99%

“…2001) did not produce any changes in the rate of spontaneous apoptosis in human neuroblastoma SH‐SY5Y cells. RA and sodium butyrate treatment of normal SVC1 and ras‐transformed Ki‐SVC1 epithelial cells resulted in a marked increase in tTG gene expression, growth arrest and differentiation but without any apoptotic features (Buommino et al . 2000).…”

mentioning

confidence: 99%

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Tissue transglutaminase differentially modulates apoptosis in a stimuli‐dependent manner

Tucholski

Johnson

2002

Journal of Neurochemistry

107

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Tissue transglutaminase is a unique member of the transglutaminase family as it not only catalyzes a transamidating reaction, but also binds and hydrolyzes GTP and ATP. Tissue transglutaminase has been reported to be pro-apoptotic, however, conclusive evidence is still lacking. To elucidate the role of tissue transglutaminase in the apoptotic process human neuroblastoma SH-SY5Y cells were stably transfected with vector only (SH/pcDNA), wild-type tissue transglutaminase (SH/tTG) and tissue transglutaminase that has no transamidating activity but retains its other functions (SH/C277S). In these studies three different apoptotic stimuli were used osmotic stress, staurosporine treatment and heat shock to delineate the role of tissue transglutaminase as a transamidating enzyme in the apoptotic process. In SH/tTG cells, osmotic stress and staurosporine treatments resulted in significantly greater caspase-3 activation and apoptotic nuclear changes then in SH/pcDNA or SH/C277S cells. This potentiation of apoptosis in SH/tTG cells was concomitant with a significant increase in the in situ transamidating activity of tissue transglutaminase. However, in the heat shock paradigm, which did not result in any increase in the transamidating activity in SH/tTG cells, there was a significant attenuation of caspase-3 activity, LDH release and apoptotic chromatin condensation in SH/tTG and SH/C277S cells compared with SH/pcDNA cells. These findings indicate for the first time that the effect of tissue transglutaminase on the apoptotic process is highly dependent on the type of the stimuli and how the transamidating activity of the enzyme is affected. Tissue transglutaminase facilitates apoptosis in response to stressors that result in an increase in the transamidating activity of the enzyme. However, when the stressors do not result in an increase in the transamidating activity of tissue transglutaminase, than tissue transglutaminase can ameliorate the apoptotic response through a mechanism that is independent of its transamidating function. Further, neither the phosphatidylinositol-3-kinase pathway nor the extracellular-regulated kinase pathway is downstream of the modulatory effects of wild-type tissue transglutaminase or C277S-tissue transglutaminase in the apoptotic cascade.

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“…1998; Tucholski et al . 2001) or rat epithelial SVC1 (Buommino et al . 2000) cells does not induce apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…1997), differentiation (Aeschlimann et al . 1993; Buommino et al . 2000), wound healing (Haroon et al .…”

mentioning

confidence: 99%

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Tissue transglutaminase differentially modulates apoptosis in a stimuli‐dependent manner

Tucholski

Johnson

2002

Journal of Neurochemistry

107

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“…The cells were lysed using 0·2% sodium dodecyl sulphate (SDS), 100 µg mL −1 RNase in TNE buffer [150 mmol L −1 sodium chloride, 10 mmol L −1 ethylenediamine tetraacetic acid (EDTA), 10 mmol L −1 Tris–HCl, pH 8], and 100 µg mL −1 of proteinase K were added to the lysate for 2·5 h at 56 °C. The high molecular weight genomic DNA, extracted from proteinase K‐treated lysates, 29 was analysed by electrophoresis in ethidium bromide‐containing 1% agarose gel in TBE (0·045 mol L −1 Tris‐borate, 0·001 mol L −1 EDTA, pH 8·0).…”

Section: Dna Fragmentation Assaymentioning

confidence: 99%

Early vitronectin receptor downregulation in a melanoma cell line during all-trans retinoic acid-induced apoptosis

Baroni¹,

Paoletti

Silvestri³

et al. 2003

Br J Dermatol

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Altogether, our data indicate that treatment of M14 melanoma cells with ATRA downregulates VnR expression and that this reduction is closely correlated with the ATRA-dependent inhibition of actin-fibre organization, cell adhesion and migration. Although the mechanism by which ATRA regulates the expression of VnR in M14 melanoma cells needs further elucidation, this system may represent a model for understanding the molecular basis of ATRA therapy in melanoma.

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“…In several studies, the life-extending capacity was also shown for sodium butyrate (SB), a short chain fatty acid having HDAC inhibition activity and known to markedly influence the processes of cell growth, differentiation and apoptosis in both normal and transformed cells (Buommino et al 2000;Khan and Jena 2014). The epigenetic modifications potentially involved in the SB-induced life extension in Drosophila have been deeply studied in a series of experiments of the research group headed by Bai-Qu Huang in the Northeast Normal University, Changchun, China (see Table 11.3).…”

Section: Sodium Butyratementioning

confidence: 99%

Life Extension

Bourg

2015

Healthy Ageing and Longevity

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Sodium butyrate/retinoic acid costimulation induces apoptosis-independent growth arrest and cell differentiation in normal and ras-transformed seminal vesicle epithelial cells unresponsive to retinoic acid

Abstract: Retinoic acid (RA) and sodium butyrate (NaB) are regulators of cell growth and differentiation. We studied their effect on normal (SVC1) or v-Ki-rastransformed (Ki-SVC1) rat seminal vesicle (SV) epithelial cell lines. The treatment of these cells with 10 7

Cited by 16 publications

References 48 publications

Tissue transglutaminase differentially modulates apoptosis in a stimuli‐dependent manner

Tissue transglutaminase differentially modulates apoptosis in a stimuli‐dependent manner

Early vitronectin receptor downregulation in a melanoma cell line during all-trans retinoic acid-induced apoptosis

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