Inhibition of growth and squamous‐cell differentiation markers in cultured human head and neck squamous carcinoma cells by β‐all‐trans retinoic acid

Jetten, Anton M.; Kim, Jun; Sacks, Peter G.; Rearick, James I.; Lotan, Dafna; Hong, Waun Ki; Lotan, Reuben

doi:10.1002/ijc.2910450135

Cited by 73 publications

(46 citation statements)

References 53 publications

(57 reference statements)

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“…Therefore, it is still unclear at which concentration RA starts to protect. The mechanism of action of retinoids on tumours appears to be related to their effect on the proliferation and differentiation of the tumour cells themselves (Lippman et al, 1987;Jetten et al, 1990;Lotan, 1994;LiaudetCoopman et al, 1997). The present study shows that two other mechanisms may be involved in attenuation of gastric carcinogenesis enhanced by sodium chloride.…”

Section: Discussionmentioning

confidence: 99%

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

et al. 1999

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The effect of prolonged administration of all- trans -retinoic acid (RA) on sodium chloride-enhanced gastric carcinogenesis induced by N -methyl- N ′-nitro- N -nitrosoguanidine, and the labelling and apoptotic indices and immunoreactivity of transforming growth factor (TGF) α in the gastric cancers was investigated in Wistar rats. After 25 weeks of carcinogen treatment, the rats were given chow pellets containing 10% sodium chloride and subcutaneous injections of RA at doses of 0.75 or 1.5 mg kg −1 body weight every other day. In week 52, oral supplementation with sodium chloride significantly increased the incidence of gastric cancers compared with the untreated controls. Long-term administration of RA at both doses significantly reduced the incidence of gastric cancers, which was enhanced by oral administration of sodium chloride. RA at both doses significantly decreased the labelling index and TGF-α immunoreactivity of gastric cancers, which were enhanced by administration of sodium chloride, and significantly increased the apoptotic index of cancers, which was lowered by administration of sodium chloride. These findings suggest that RA attenuates gastric carcinogenesis, enhanced by sodium chloride, by increasing apoptosis, decreasing DNA synthesis, and reducing TGF-α expression in gastric cancers. © 1999 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 99%

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

et al. 1999

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“…Retinoids have a broad spectrum of anti-proliferative activity in cultured cell systems, particularly transformed cells and are used in the therapy of certain hyper-proliferative, pre-malignant and malignant diseases (Gudas et al, 1994). In addition retinoids alter the differentiation of many cell types, inhibiting squamous differentiation in epithelial cells (Jetten et al, 1990) and inducing the differentiation of myeloid cells (Robertson et al, 1992b). These activities underlie their use in the treatment of leukemias and certain squamous cancers.…”

Section: Retinoid Receptors and Apoptosismentioning

confidence: 99%

Retinoid-induced apoptosis in normal and neoplastic tissues

Thomázy²,

et al. 1998

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Vitamin A and its derivatives (collectively referred to as retinoids) are required for many fundamental life processes, including vision, reproduction, metabolism, cellular differentiation, hematopoesis, bone development, and pattern formation during embryogenesis. There is also considerable evidence to suggest that natural and synthetic retinoids have therapeutical effects due to their antiproliferative and apoptosis-inducing effectsin human diseases such ascancer. Therefore it is not surprising that a significant amount of research was dedicated to probe the molecular and cellular mechanisms of retinoid action during the past decade. One of the cellular mechanisms retinoids have been implicated in is the initiation and modulation of apoptosis in normal development and disease. This review provides a brief overview of the molecular basis of retinoid signaling, and focuses on the retinoid-regulation of apoptotic cell death and gene expression during normal development and in pathological conditions in vivo and in various tumor cell lines in vitro.Keywords: retinoic acid; retinoic acid receptor; RAR; RXR; apoptosis; tissue transglutaminase; gene expression Abbreviations: ATRA, All-trans retinoic acid; 9-cis RA, 9-cis retinoic acid; PG-J 2 , 15-deoxy-D 12,14 PGJ 2 ; RAR, retinoic acid receptor; RXR, retinoid X receptor; Tgase, tissue transglutaminase; SMRT, silencing mediator of retinoid and thyroid receptors; N-CoR, nuclear receptor corepressor; CREB, creb binding protein; HDAC-1, histone deacetylase-1 Retinoids are modulators of transcriptionThe retinoid's mechanism of action in both normal and pathological conditions has been the subject of more than a decade of intense research. The cloning and discovery of the retinoic acid receptor (RAR), which belongs to the superfamily of ligand-activated transcription factors (nuclear receptors) revolutionized our understanding as to how retinoids exert their pleiotropic effects (for reviews see Chambon (1996);Mangelsdorf et al (1994)). Members of the nuclear receptor superfamily mediate the biological effects of many hormones, vitamins and drugs (i.e. steroid hormones, thyroid hormones, vitamin D, prostaglandin-J 2 (PG-J 2 ) and drugs that activate peroxisomal proliferation). There are two families of retinoid receptors, Retinoid X Receptors (RXRs) that bind 9-cis retinoic acid (9-cis RA) and Retinoic Acid Receptors (RARs) that bind both 9-cis RA and all-trans retinoic acid (ATRA) (for reviews see Chambon 1996;Mangelsdorf et al, 1994)). Each of these receptor families includes at least three distinct genes, (RARa,b and g; RXRa,b and g) that through differential promoter usage and alternative splicing, give rise to a large number of distinct retinoid receptor proteins (for reviews see

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“…Retinoids, natural and synthetic vitamin A metabolites and analogues, inhibit the proliferation of several types of tumour cells, such as head and neck squamous cell carcinoma (SCC) (Jetten et al, 1990;Lotan, 1994;Oridate et al, 1996), oesophageal cancer (Xu et al, 1999), lung cancer (Zou et al, 1998;Sun et al, 1999a,b), prostate cancer (Sun et al, 1999c), and cervical cancer Oridate et al, 1997). The effects of retinoids are mediated by both nuclear retinoid receptors (RARs and RXRs) and cytoplasmic retinoic acid binding proteins (CRABP1 and CRABP2) (Pemrick et al, 1994).…”

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confidence: 99%

Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines

et al. 2001

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Summary Retinoids inhibit the proliferation of several types of tumour cells, and are used for patients with several malignant tumours. In this study, we examined the effect of retinoic acids (RAs) on the invasive potentials of the oral squamous cell carcinoma (SCC) cells, BHY and HNt. BHY cells expressed all of retinoid nuclear receptors (RARα, β, γ, and RXRα) and cytoplasmic retinoic acid binding proteins (CRABP1 and CRABP2). HNt cells lacked the expression of RARβ, but expressed other nuclear receptors and CRABPs. All-trans retinoic acid (ATRA) and 13-cis retinoic acid (13-cisRA) (10 -6 and 10 -7 M) inhibited the growth of the cells, but low-dose ATRA and 13-cisRA (10 -8 M) marginally affected the growth of the cells. Surprisingly, low-dose RAs enhanced the activity of tissue-type plasminogen activator (tPA), and activated pro-matrix metalloproteinases (proMMP2 and proMMP9). Activation of proMMP2 and proMMP9 was inhibited by aprotinin, a serineproteinase, tPA inhibitor. MATERIALS AND METHODS Cells and cell cultureBHY and HNt (Kawamata et al, 1997) cells were derived from human oral SCC tumours from patients. HT1080 cells are a human fibrosarcoma cell line purchased from Dai-Nippon Seiyaku, Osaka, Japan. All of the cells were maintained in DMEM (Life Technologies, Inc, Gaithersburg, MD) supplemented with 10% FCS (Bio-Whittaker, Walkersville, MD), 100 µg ml -1 streptomycin, and 100 U ml -1 penicillin, 0.25 µg ml -1 Amphotericin B (Life Technologies, Inc.) in a humidified atmosphere of 95% air and 5% CO 2 at 37˚C. MTT assayWe examined the effect of ATRA (Sigma, St. Louis, MO) and 13-cisRA (Sigma) on the growth of the cells by an assay in which MTT (Sigma) was used. Cells were seeded on a 96-well plate (Falcon; Becton Dickinson Labware, Lincoln Park, NJ) at 5 × 10 3 cells per well in DMEM containing 10% FCS. After 24 h, cells were washed twice with DMEM without FCS and cultured in DMEM without FCS in the presence or absence of ATRA (10 -6 , 10 -7 and 10 -8 M) or 13-cisRA (10 -6 , 10 -7 and 10 -8 M). After 3 days, the number of cells was quantitated by MTT assay (Carmichael et al, 1987). Gelatinase zymography and reverse gelatinase zymographyCells were grown to confluence in 60 mm dishes (Falcon) in the serum-supplemented medium, washed twice with serum-free DMEM, and cultured in 3 ml of serum-free DMEM in the presence or absence of ATRA (10 -8 M) or 13-cisRA (10 -8 M) for an additional 48 h. The medium was collected, clarified by centrifugation at 1800 g, and concentrated down to 0.1 ml approximately 30-fold by Centricon 10 (cut-off, Mr 10 000; Millipore Corp, Bedford, MA). We have already confirmed that the process of the protein concentration did not activate the progelatinases in the samples (Kawamata et al, 1997). The protein concentration of the samples are determined by Bio-Rad protein assay (Bio-Rad, Hercules, CA). The gels for zymorgraphy were composed of gelatin (0.1%; Sigma) and polyacrylamide (10%), and for reverse zymography, of gelatin (0.1%), polyacrylamide (12.5%) and concentrated conditioned medi...

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Inhibition of growth and squamous‐cell differentiation markers in cultured human head and neck squamous carcinoma cells by β‐all‐trans retinoic acid

Cited by 73 publications

References 53 publications

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

Retinoid-induced apoptosis in normal and neoplastic tissues

Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines

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