Expression of Src-like Adapter Protein mRNA Is Induced by All-trans Retinoic Acid

Ohtsuki, T.; Hatake, Kiyohiko; Ikeda, Masayuki; Tomizuka, Hiroshi; Terui, Yasuhito; Uwai, Masaya; Miura, Yasusada

doi:10.1006/bbrc.1996.5887

Cited by 18 publications

(13 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The induction of apoptosis after combined treatment with 5-Aza-dCyd and ATRA is possibly explained by retinoic acid acting on the demethylated cell population generated after 5-Aza-dCyd treatment. The K562 cell lines was previously reported to be resistant to differentiation induction by ATRA (23,24). Similar results were obtained when we studied other cell lines, such as the breast cancer cell lines CAMA-1 and BT-474, but using 1 M of ATRA after only 0.1 M of 5-Aza-dCyd instead of 1 M as in the cell line K562.…”

Section: Discussionsupporting

confidence: 87%

Hypermethylation and Silencing of the Putative Tumor SuppressorTazarotene-Induced Gene 1in Human Cancers

Youssef¹,

Chen²,

Higuchi

et al. 2004

Cancer Research

View full text Add to dashboard Cite

A variety of tumor suppressor genes are down-regulated by hypermethylation during carcinogenesis. Using methylated CpG amplificationrepresentation difference analysis, we identified a DNA fragment corresponding to the Tazarotene-induced gene 1 (TIG1) promoter-associated CpG island as one of the genes hypermethylated in the leukemia cell line K562. Because TIG1 has been proposed to act as a tumor suppressor, we tested the hypothesis that cytosine methylation of the TIG1 promoter suppresses its expression and causes a loss of responsiveness to retinoic acid in some neoplastic cells. We examined TIG1 methylation and expression status in 53 human cancer cell lines and 74 primary tumors, including leukemia and head and neck, breast, colon, skin, brain, lung, and prostate cancer. Loss of TIG1 expression was strongly associated with TIG1 promoter hypermethylation (P < 0.001). There was no correlation between TIG1 promoter methylation and that of retinoid acid receptor ␤2 (RAR␤2), another retinoic-induced putative tumor suppressor gene (P ‫؍‬ 0.78). Treatment with the DNA methyltransferase inhibitor 5-aza-2-deoxycytidine for 5 days restored TIG1 expression in all eight silenced cell lines tested. TIG1 expression was also inducible by treatment with 1 M all-trans-retinoic acid for 3 days except in densely methylated cell lines. Treatment of the K562 leukemia cells with demethylating agent combined with all-trans-retinoic acid induced apoptosis. These findings indicate that silencing of TIG1 promoter by hypermethylation is common in human cancers and may contribute to the loss of retinoic acid responsiveness in some neoplastic cells.

show abstract

Section: Discussionsupporting

confidence: 87%

Hypermethylation and Silencing of the Putative Tumor SuppressorTazarotene-Induced Gene 1in Human Cancers

Youssef¹,

Chen²,

Higuchi

et al. 2004

Cancer Research

View full text Add to dashboard Cite

show abstract

“…For instance, SLAP expression is induced following dexamethasone treatment of mast cells and in lymphoma cell lines undergoing differentiation in response to retinoic acid (17,18). In addition, SLAP expression is upregulated in Friend leukemia virus integration-1-transformed erythroblast cells, and it inhibits erythropoietin-induced differentiation of these cells (19).…”

Section: Endritic Cells (Dc)mentioning

confidence: 99%

The Src-Like Adaptor Protein Regulates GM-CSFR Signaling and Monocytic Dendritic Cell Maturation

Liontos

Dissanayake

Ohashi

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

GM-CSF is an important cytokine involved in myeloid differentiation and inflammatory processes. Signaling through the GM-CSFR also plays a critical role in the generation of monocyte-derived dendritic cells (DC). In this article, we report that the Src-like adaptor protein (SLAP) functions as a negative regulator of the GM-CSFR. In bone marrow-derived DC (BM-DC) lacking SLAP and the closely related SLAP2, downregulation of GM-CSFRβ is impaired, leading to enhanced phosphorylation of Jak2 and prolonged activation of Akt and Erk1/2 in response to GM-CSF stimulation. Compared with wild-type bone marrow, SLAP/SLAP2−/− bone marrow gave rise to similar numbers of CD11c+ and CD11b+ DC, but SLAP/SLAP2−/− BM-DC failed to acquire high levels of MHC class II, CD80, and CD86, indicating an impairment in maturation. Furthermore, MHC class II expression in SLAP/SLAP2−/− BM-DC was rescued by decreasing GM-CSF concentration, suggesting that enhanced GM-CSF signaling mediates the block in maturation. In addition, SLAP/SLAP2−/− BM-DC produced less IL-12 and TNF-α in response to LPS compared with controls and failed to stimulate T cells in an MLR. Ag-specific T cell activation assays showed that SLAP/SLAP2−/− BM-DC were less robust at inducing IFN-γ secretion by DO11.10 T cells. These results indicated that SLAP-mediated GM-CSFR regulation is important for the generation of functionally mature monocytic DC.

show abstract

“…The annealing temperature and reaction cycles for the different components were programmed as follows: 59°C and 39 cycles for factor B, 63°C and 40 cycles for CD11c, 55°C and 40 cycles for CD35, and 55°C and 30 cycles for ␤-actin. Amplification products were analyzed by electrophoresis in a 2% agarose gel using 1ϫ Tris acetate EDTA (TAE) and visualized with 0.1 g/mL ethidium bromide staining, as performed in our previous study (Ohtsuki et al, 1997).…”

Section: Reverse Transcription-polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

A new apoptotic pathway for the complement factor B-derived fragment Bb

et al. 2000

Self Cite

View full text Add to dashboard Cite

Apoptosis is involved in both the cellular and humoral immune system destroying tumors. An apoptosis-inducing factor from HL-60 myeloid leukemia cells was obtained, purified, and sequenced. The protein found has been identified as a human complement factor B-derived fragment Bb, although it is known that factor B is able to induce apoptosis in several leukemia cell lines. Monoclonal antibodies against fragment Ba and Bb inhibited the apoptotic activity of factor B. When the purified fragment Bb was used for apoptosis induction, only the anti-Bb antibody inhibited Bb-induced apoptosis, and not the anti-Ba antibody. The apoptosis-inducing activity was found to be enhanced under conditions facilitating the formation of Bb. Blocking TNF/TNFR or FasL/Fas interactions did not interfere with the factor B-induced apoptosis. CD11c (iC3bR) acts as the main subunit of a heterodimer binding to fragment Bb in the apoptosis pathway, and the factor B-derived fragment Bb was found to possess the previously unknown function of inducing apoptosis in leukemic cells through a suicide mechanism of myeloid lineage cells during the differentiation stage.

show abstract

Expression of Src-like Adapter Protein mRNA Is Induced by All-trans Retinoic Acid

Cited by 18 publications

References 15 publications

Hypermethylation and Silencing of the Putative Tumor SuppressorTazarotene-Induced Gene 1in Human Cancers

Hypermethylation and Silencing of the Putative Tumor SuppressorTazarotene-Induced Gene 1in Human Cancers

The Src-Like Adaptor Protein Regulates GM-CSFR Signaling and Monocytic Dendritic Cell Maturation

A new apoptotic pathway for the complement factor B-derived fragment Bb

Contact Info

Product

Resources

About