HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter

Stable Identifier
R-HSA-9825754
Type
Reaction [binding]
Species
Homo sapiens
Compartment
nucleoplasm
ReviewStatus
5/5
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HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter
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HINT1 is a repressor of MITF activity that binds to the BCL2 and CCND1 promoters in melanoma cells as assessed by ChIP. Expression of HINT1 decreases expression of BCL2 and CCND1 reporter genes in melanoma cell lines, and cells treated with anti-HINT1 siRNA show elevated levels of BCL2 and CCND1 mRNA and protein. HINT1 co-immunoprecipitates with both MITF and also with the transcriptional co-repressors SIN3A and HDAC1. Overexpression of HINT1 causes a decrease in cellular proliferation, promotes apoptosis and reduces tumor formation in nude mice; these effects are partially reversed upon ectopic expression of BCL2 and CCND1 (Genovese et al, 2012; reviewed in Hartman and Czyz, 2015).
Literature References
PubMed ID Title Journal Year
25142731 Pro-survival role of MITF in melanoma

Hartman, ML, Czyz, M

J Invest Dermatol 2015
22647378 The tumor suppressor HINT1 regulates MITF and β-catenin transcriptional activity in melanoma cells

Sioletic, S, Sgambato, A, Cittadini, A, Rettino, A, Ghosh, P, Genovese, G, Li, H

Cell Cycle 2012
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Orthologous Events
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Bos taurus)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Caenorhabditis elegans)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Canis familiaris)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Drosophila melanogaster)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Gallus gallus)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Mus musculus)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Rattus norvegicus)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Sus scrofa)
HINT1, SIN3A and HDAC1 bind MITF-M at the BCL2 promoter (Xenopus tropicalis)
Authored
Rothfels, K  (2023-01-26)
Reviewed
de la Serna, IL  (2024-05-21)
Arnheiter, H  (2024-02-26)
Created
Rothfels, K  (2023-01-26)
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