tretinoin has been researched along with Salivary-Gland-Neoplasms* in 11 studies
1 review(s) available for tretinoin and Salivary-Gland-Neoplasms
1 trial(s) available for tretinoin and Salivary-Gland-Neoplasms
10 other study(ies) available for tretinoin and Salivary-Gland-Neoplasms
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Increased retinoic acid signaling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway.
MYB-NFIB fusion and NOTCH1 mutation are common hallmark genetic events in salivary gland adenoid cystic carcinoma (SACC). However, abnormal expression of MYB and NOTCH1 is also observed in patients without MYB-NFIB fusion and NOTCH1 mutation. Here, we explore in-depth the molecular mechanisms of lung metastasis through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near-normal to cancer-based on the abundance of each cell cluster in normal tissue. In this context, we identified the Notch signaling pathway enrichment in almost all cancer cells; RNA velocity, trajectory, and sub-clustering analyses were performed to deeply investigate cancer progenitor-like cell clusters in primary tumor-associated lung metastases, and signature genes of progenitor-like cells were enriched in the "MYC_TARGETS_V2" gene set. In vitro, we detected the NICD1-MYB-MYC complex by co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) as an endogenous antagonist of genes in the "MYC_TARGETS_V2" gene set. Following this, we confirmed that all-trans retinoic acid (ATRA) suppresses the lung metastasis of SACC by correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic, RNA-seq, and immunohistochemical (IHC) analyses of primary tissues and metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of the RA system in diagnosis and treatment. Topics: Carcinoma, Adenoid Cystic; Humans; Lung Neoplasms; Receptor, Notch1; Salivary Gland Neoplasms; Signal Transduction; Tretinoin | 2023 |
Zebrafish blastomere screen identifies retinoic acid suppression of
Pluripotent cells have been used to probe developmental pathways that are involved in genetic diseases and oncogenic events. To find new therapies that would target Topics: Animals; Blastomeres; Carcinoma, Adenoid Cystic; Humans; Mice; Mice, Nude; Proto-Oncogene Proteins c-myb; Salivary Gland Neoplasms; Tretinoin; U937 Cells; Xenograft Model Antitumor Assays; Zebrafish; Zebrafish Proteins | 2018 |
Expression of cAMP response element binding protein (CREB)-binding protein (CBP) and the implication in retinoic acid-inducible transcription activation in human salivary gland adenocarcinoma cell line HSG.
In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. In order to investigate the relationship of CBP to the RA signaling in a human salivary gland (HSG) adenocarcinoma cell line, we examined the expression of CBP in the cells. Immunoprecipitation and immunoblotting of the nuclear extract of HSG cells with anti-human CBP antibody showed a specific 270-kDa band, indicating the expression of CBP in HSG cells. The immunocytochemical analysis confirmed the nuclear localization of CBP. The transfection of HSG cells with a luciferase reporter plasmid harboring an RA-response element at the 5'-upstream region of the reporter gene increased RA-dependent luciferase activity approximately 3-fold. Co-transfection with a CBP-expression plasmid and the luciferase reporter gene enhanced the RA-dependent transcription activation approximately 10-fold. The immunoprecipitates obtained with anti-CBP antibody exhibited a histone acetyl-transferase (HAT) activity 2-fold higher than that obtained with the control antibody, whereas the HAT activity of the immunoprecipitates with anti-SRC-1 and anti-p/CIP, which were used as comparisons, were only a little increased. The RA treatment had no effect on the level of HAT activity except in the case of using the immunoprecipitate obtained with anti-RARalpha, in which case it increased the activity. These findings indicate that CBP expressed in HSG cells mediates the RA-inducible growth and differentiation-regulating transcription activation in concert with the retinoic acid receptors. Topics: Acetyltransferases; Adenocarcinoma; Cell Line, Tumor; CREB-Binding Protein; Genes, Reporter; Histone Acetyltransferases; Humans; Immunohistochemistry; Nuclear Proteins; Precipitin Tests; Receptors, Retinoic Acid; Response Elements; Salivary Gland Neoplasms; Signal Transduction; Trans-Activators; Transcriptional Activation; Transfection; Tretinoin | 2003 |
Inhibition of retinoic acid-inducible transcription by COUP-TFI in human salivary gland adenocarcinoma cell line HSG.
Human salivary gland adenocarcinoma cells (HSG) express nuclear receptors, all-trans-retinoic acid (at-RA) receptors (RARs), and retinoid X/9-cis-retinoic acid (9-c-RA) receptors (RXRs). In order to investigate whether the endogenous RARs or RXRs of HSG cells can induce transcription activation, the thymidine kinase promoter (TK)-driven luciferase reporter gene containing the retinoic acid response element (RARE), of RARbeta, betaRARE2-TK-Luc, was transfected into HSG cells and ligand-dependent transcription activation was examined. Luciferase activity of cell lysate increased by the treatment with either at-RA or 9-c-RA. Co-transfection of RARalpha and (or) RXRalpha-expression plasmids with the reporter gene enhanced the luciferase activity, suggesting that endogenous RARs and RXRs work as ligand-dependent transfactors in HSG cells. Reverse transcriptase - polymerase chain reaction analysis revealed that HSG cells express chicken ovalbumin upstream promoter - transcription factor I (COUP-TFI). Co-transfection of COUP-TFI-expression plasmid suppressed the at-RA-induced transcription activation of the reporter gene. Similar results were shown using a chromatin-integrated reporter gene system, using a stably transfected beta-RARE2-TK-beta-galactosidase (beta-Gal) reporter gene. The at-RA-dependent increase in the beta-Gal expression was completely inhibited by COUP-TFI. The transfection of antisense oligonucleotide of COUP-TFI squelched the RA-dependent growth inhibition induced by RAR-RXR heterodimers. Conclusively, RARs and RXRs of HSG cells are functional and play roles as transactivators in at-RA-sensitive processes such as the proliferation or differentiation of cells. COUP-TFI very likely regulates these processes by repressing the functions of these transactivators. Topics: Adenocarcinoma; Animals; Cell Division; COUP Transcription Factor I; DNA-Binding Proteins; Humans; Ligands; Rats; Receptors, Retinoic Acid; Response Elements; Reverse Transcriptase Polymerase Chain Reaction; RNA, Antisense; Salivary Gland Neoplasms; Transcription Factors; Transcription, Genetic; Tretinoin; Tumor Cells, Cultured | 1999 |
Retinoic acid enhances expression of bone morphogenetic protein-2 in human adenocarcinoma cell line (HSG-S8).
Expression of bone morphogenetic protein (BMP)-2 mRNA was stimulated by retinoic acid in human adenocarcinoma cell line, HSG-S8, in a dose-dependent manner. Northern blot analysis demonstrated that retinoic acid most strongly increased the level of BMP-2 mRNA 6 h after the treatment and the stimulatory effect was maintained at 48 h. The mature peptides of 16 and 18 kDa molecular masses of BMP-2 were also increased in the conditioned medium by the treatment of retinoic acid on western blotting. The proliferation of HSG-S8 cells was inhibited by retinoic acid, however, retinoic acid did not cause morphological change showing cellular differentiation. 1 alpha, 25(OH)2D3, like retinoic acid, clearly increased the mRNA level of BMP-2, whereas dibuthryl cyclic AMP remarkably diminished it, and bromodeoxyuridine had no effect on the expression of BMP-2 mRNA. Topics: Adenocarcinoma; Blotting, Western; Bone Morphogenetic Proteins; Bucladesine; Calcitriol; Culture Media, Serum-Free; Humans; Protein Biosynthesis; RNA, Messenger; Salivary Gland Neoplasms; Stimulation, Chemical; Thymidine; Tretinoin; Tritium; Tumor Cells, Cultured | 1996 |
Effect of individual and multiple antioxidant vitamins on growth and morphology of human nontumorigenic and tumorigenic parotid acinar cells in culture.
The effects of individual and multiple antioxidant vitamins on growth and morphology of human nontumorigenic (2HPC8) and tumorigenic (2HP1G) parotid acinar cells in culture have not been investigated. Our study showed that tumorigenic acinar cells were more sensitive than nontumorigenic acinar cells to individual vitamins such as vitamin C, beta-carotene (BC), d-alpha-tocopheryl succinate (alpha-TS), and retinoic acid (RA) and a mixture of four vitamins (vitamin C, BC, alpha-TS, and RA). The effect of individual vitamins on tumorigenic acinar cells depended on the dose and the type of vitamins. Vitamin C at a low concentration stimulated growth, but at a high concentration it inhibited growth. BC was most effective in reducing growth, and it alone caused extensive morphological changes in tumorigenic acinar cells. A mixture of four vitamins at appropriate doses was more effective than a mixture of two or three vitamins at the same doses in reducing the growth of tumorigenic acinar cells. The extent of growth inhibition depended on the dose and the type of vitamins. Our results suggest that the use of multiple antioxidant vitamins is essential for a maximal reduction in cancer incidence among a high-risk population. The use of one or two vitamins may be ineffective or even harmful. Topics: Antioxidants; Ascorbic Acid; beta Carotene; Cells, Cultured; Humans; Parotid Gland; Salivary Gland Neoplasms; Tocopherols; Tretinoin; Vitamin E; Vitamins | 1996 |
[Proliferation and differentiation of human salivary gland adenocarcinoma cell line HSG].
The adenocarcinoma cell line derived from an intercalated ductal epithelium of a human salivary gland (HSG) proliferates autonomously mediated by an epidermal growth factor-(EGF)-like molecule with a molecular weight of 46 kDa and an EGF receptor (EGFR). The c-erbB2 protein, a member of EGFR family was also expressed in HSG cells and was involved in the growth signal pathway of HSG cells as well as EGFR. The autocrine growth is regulated by glucocorticoid and retinoic acid (RA) via their receptors. Retinoic acid receptor (RAR) of HSG cells revealed a transcriptional activity in vivo, and the heterodimerization between RAR and 9-cis retinoic acid receptor (RXR) is requisite for the binding with a specific DNA element termed RA response element in vitro. RXR alpha and RXR beta were cloned from HSG cells, and these RXRs, together with RAR, seemed to play a physiological role in RA signaling in vivo. Topics: Adenocarcinoma; Bucladesine; Cell Division; Cell Transformation, Neoplastic; Epidermal Growth Factor; Humans; Receptors, Retinoic Acid; Salivary Gland Neoplasms; Signal Transduction; Transcription, Genetic; Tretinoin; Tumor Cells, Cultured | 1996 |
Retinoic acid receptor in subclone of human salivary gland adenocarcinoma cell line HSG and effect of retinoic acid on cellular growth.
Retinoic acid (RA) binding has been detected in the nuclei of a subclone (CL-1) of human submandibular adenocarcinoma cell line HSG conditioned to grow in a serum-free defined medium. Competition assay confirmed the specificity of the RA binding. Scatchard analysis showed the binding molecule to have a high affinity and low capacity. From the analyses by gel-filtration and glycerol density gradient centrifugation, the nuclear binding molecule appears to be distinct from cellular RA binding protein (CRABP) in terms of molecular weight. Furthermore, immunoblotting analysis revealed a band (Mr 47,000) reactive with specific antibody to RA receptor (RAR) alpha in the gel containing the nuclear fraction of CL-1 cells. Northern blotting analysis with specific cDNA probes revealed the expression of RAR alpha and RAR gamma in CL-1 cells. These results indicate that CL-1 cells express two types of RAR subtype, suggesting that these receptor molecules may mediate biological effects of RA. Treatment of CL-1 cells with RA resulted in an increase in the incorporation of [3H]thymidine into TCA-insoluble materials. The maximal increase was observed at 10(-6) M around 48 h. Previously, we demonstrated the autocrine growth of HSG cells mediated by epidermal growth factor (EGF) receptors and EGF-like molecules (Kurokawa et al. (1989) Cancer Res. 49, 5136-5142) and showed that RA had no significant effect on the secretion of the EGF-like molecule. RA induced an increase in [125I]EGF binding to CL-1 cells. The increase in the EGF binding was maximal at 24 h at 10(-6) M RA. RA also increased the amount of [3H]leucine-labeled EGF receptor dose-dependently. No significant change was observed in total protein synthesis of CL-1 cells by treatment with RA. These results suggest that RA stimulates the growth of CL-1 cells by increasing EGF receptor levels. Topics: Adenocarcinoma; Carrier Proteins; Cell Division; Cell Nucleus; Clone Cells; DNA, Neoplasm; Epidermal Growth Factor; ErbB Receptors; Humans; Receptors, Retinoic Acid; RNA, Messenger; Salivary Gland Neoplasms; Tretinoin; Tumor Cells, Cultured | 1991 |
Effects of retinoic acid on morphological features and biological markers of a neoplastic human salivary intercalated duct cell line in culture.
Retinoic acid has marked effects on the growth, morphological features, and biological markers of a neoplastic human salivary intercalated duct cell clone in culture, whereas the cell clone was not affected by other retinoids such as retinol and retinal. A cell clone with ultrastructure and biological markers specific to the intercalated duct cells of human salivary glands was cultivated in the presence of retinoic acid. Major alterations, such as expression of tonofilaments, Mr 68,000 cytokeratin, and involucrin, were observed in those cells with a phenotype similar to that of keratinizing squamous cells. In addition, the coexpression of Mr 68,000 cytokeratin and carcinoembryonic antigen in these altered cells was found. Both the anchorage-independent and anchorage-dependent growths were markedly suppressed in the presence of retinoic acid. After the removal of retinoic acid from the culture, the treated cells returned rapidly to the phenotype of the untreated cells. These findings indicate that reversible differentiation into the keratinizing squamous cells of a neoplastic human salivary intercalated duct cell clone occurs in growth medium containing retinoic acid. Topics: Adenocarcinoma; Biomarkers, Tumor; Carcinoembryonic Antigen; Cell Line; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Keratins; Microscopy, Electron; Molecular Weight; Salivary Gland Neoplasms; Tretinoin | 1988 |
Chemopreventive effects of beta-carotene and 13-cis-retinoic acid on salivary gland tumors.
The chemopreventive effects of beta-carotene and 13-cis-retinoic acid (RA) on chemically induced salivary gland tumors were studied in rats. Young male Sprague-Dawley rats were injected in one of the submandibular salivary glands with 1 mg of dimethylbenzanthracene (DMBA) dissolved in olive oil. The contralateral gland was injected with the vehicle alone. Rats were divided into four groups and were fed ad libitum a semisynthetic diet supplemented with 0 or 100 mg beta-carotene/kg diet, or 20 or 100 mg RA/kg diet. Rats were killed at 22 weeks after the DMBA treatment, and tumors were examined histologically. Tumors were generally found to be squamous cell carcinomas or poorly differentiated neoplasms resembling squamous cell carcinomas. The tumor incidence was slightly lower in rats fed the diet supplemented with beta-carotene. RA had no appreciable effect on tumor incidence. A high activity of gamma-glutamyl transpeptidase was histochemically demonstrated in the tumors. There were some mortalities in the beta-carotene and RA supplemented groups, especially in the group fed high levels of RA. This mortality appeared to be related to vitamin K becoming somewhat limited. Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; beta Carotene; Butylated Hydroxytoluene; Carotenoids; Diterpenes; Male; Rats; Rats, Inbred Strains; Retinyl Esters; Salivary Gland Neoplasms; Submandibular Gland Neoplasms; Time Factors; Tretinoin; Vitamin A | 1984 |