The interplay between histone deacetylases and c-Myc in the transcriptional suppression of HPP1 in colon cancer

Wang, Jian; Elahi, Abul; Ajidahun, Abidemi; Clark, W. Edwin; Hernandez, Jonathan M.; Achille, Alex; Jiang, Hao; Seto, Edward; Shibata, David

doi:10.4161/cbt.29500

Cited by 17 publications

(13 citation statements)

References 32 publications

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“…As reported, c-Myc can recruit HDAC1 or HDAC3 to inhibit expression of specific genes, 19 which lead us to investigate whether the c-myc/HDAC1/3 complex was involved in the transcriptional repression of CRY2 and FBXL3. To address this hypothesis, we initially examined effects of deacetylase inhibitor Trichostatin A (TSA) on CRY2 and FBXL3 expression.…”

Section: Resultsmentioning

confidence: 95%

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

et al. 2017

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Colorectal cancer (CRC) is the second major cause of tumor-related deaths. MicroRNAs (miRNAs) have pivotal roles in CRC progression. Here, we describe the effect of miR-181d on CRC cell metabolism and underlying molecular mechanism. Our data firmly demonstrated that knockdown of miR-181d suppressed CRC cell proliferation, migration, and invasion by impairing glycolysis. Mechanistically, miR-181d stabilized c-myc through directly targeting the 3′-UTRs of CRY2 and FBXL3, which subsequently increased the glucose consumption and the lactate production. Inhibition of c-myc via siRNA or small molecular inhibitor abolished the oncogenic effects of miR-181d on the growth and metastasis of CRC cells. Furthermore, c-myc/HDAC3 transcriptional suppressor complex was found to co-localize on the CRY2 and FBXL3 promoters, epigenetically inhibit their transcription, and finally induce their downregulation in CRC cells. In addition, miR-181d expression could be directly induced by an activation of c-myc signaling. Together, our data indicate an oncogenic role of miR-181d in CRC by promoting glycolysis, and miR-181d/CRY2/FBXL3/c-myc feedback loop might be a therapeutic target for patients with CRC.

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Section: Resultsmentioning

confidence: 95%

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

et al. 2017

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“…As reported, c-Myc could recruit HDAC1 or HDAC3 to suppress expression of specific genes, such as HPP1 [26], miR-29 [27], miR-15/16-1 [28], which leads us to investigate whether the recruitment of HDAC1/3 is involved in the transcriptional repression of miR-451 by c-Myc. To address this hypothesis, we firstly examined effects of deacetylase inhibitor Trichostatin A (TSA) on miR-451 expression.…”

Section: Resultsmentioning

confidence: 99%

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

Gong

Chen

et al. 2016

Oncotarget

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Aberrant activation of c-Myc plays an important oncogenic role via regulating a series of coding and non-coding genes in acute myeloid leukemia (AML). Histone deacetylases (HDACs) can remove acetyl group from histone and regulate gene expression via changing chromatin structure. Here, we found miR-451 is abnormally down-regulated in AML patient samples; c-Myc recruits HDAC3 to form a transcriptional suppressor complex, co-localizes on the miR-451 promoter, epigenetically inhibits its transcription and finally induces its downregulation in AML. Furthermore, our in vitro and in vivo results suggest that miR-451 functions as a tumor suppressor via promoting apoptosis and suppressing malignant cell proliferation. The mechanistic study demonstrated that miR-451 directly targets YWHAZ mRNA and suppresses YWHAZ/AKT signaling in AML. Knockdown of c-Myc results in restoration of miR-451 and inhibition of YWHAZ/AKT signaling. In AML patients, low level of miR-451 is negatively correlated with high levels of c-Myc and YWHAZ, while c-Myc level is positively related to YWHAZ expression. These results suggested that c-Myc⊣miR-451⊣YWHAZ/AKT cascade might play a crucial role during leukemogenesis, and reintroduction of miR-451 could be as a potential strategy for AML therapy.

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“…All the previous tests were performed using fused peptides. To evaluate how the system performed on “real” proteins pairs or oligomers, known PPI were selected for each reporter: eGFP–foldon [ 37 ] (homotrimer of GFP), sGFP–MyD88 [ 38 ], the cMyc(b/HLH/Zip)–HDAC3 [ 39 ] pair (heterodimer of sGFP-mCherry), mCherry–SOX9 [ 40 ] (mCherry homodimer), and mCherry–Cav1 [ 32 ] ( Figure 4 ). For detecting these interacting proteins, the targets and SLNs were separately expressed in Leishmania cell-free lysate and the targets were serially diluted three-fold before adding them to the assay (detailed experiment outlined in the material and methods section).…”

Section: Resultsmentioning

confidence: 99%

A Split-Luciferase Reporter Recognizing GFP and mCherry Tags to Facilitate Studies of Protein–Protein Interactions

Moustaqil

Bhumkar

González

et al. 2017

IJMS

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The use of fluorescently-tagged proteins in microscopy has become routine, and anti-GFP (Green fluorescent protein) affinity matrices are increasingly used in proteomics protocols. However, some protein–protein interactions assays, such as protein complementation assays (PCA), require recloning of each protein as a fusion with the different parts of the complementation system. Here we describe a generic system where the complementation is separated from the proteins and can be directly used with fluorescently-tagged proteins. By using nanobodies and performing tests in cell-free expression systems, we accelerated the development of multiple reporters, detecting heterodimers and homodimers or oligomers tagged with GFP or mCherry. We demonstrate that the system can detect interactions at a broad range of concentrations, from low nanomolar up to micromolar.

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The interplay between histone deacetylases and c-Myc in the transcriptional suppression of HPP1 in colon cancer

Cited by 17 publications

References 32 publications

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

miR-181d and c-myc-mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancer

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

A Split-Luciferase Reporter Recognizing GFP and mCherry Tags to Facilitate Studies of Protein–Protein Interactions

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