We are analyzing https://link.springer.com/article/10.1007/s00109-010-0701-7.

Title:
The role of histone deacetylase 7 (HDAC7) in cancer cell proliferation: regulation on c-Myc | Journal of Molecular Medicine
Description:
Histone deacetylases (HDACs) play fundamental roles in the epigenetic regulation of gene expression and contribute to the growth, differentiation, and apoptosis of cancer cells. Although HDACs are recognized to be closely related to cancer development and altered expression of certain HDACs is observed in tumor samples, the arcane characters of HDACs in tumorigenesis have not been fully illustrated. Herein, we report that HDAC7 is a crucial player in cancer cell proliferation. Knockdown of HDAC7 resulted in significant G1/S arrest in different cancer cell lines. Subsequent investigations indicated that HDAC7 silencing blocked cell cycle progression through suppressing c-Myc expression and increasing p21 and p27 protein levels. The ectopic expression of c-Myc in turn antagonized the cell cycle arrest and repressed the elevation of p21 and p27 in HDAC7 silencing setting. Of note, HDAC7 deficiency was further identified to induce cellular senescence program, which was also reversed by c-Myc re-expression. Further chromatin immunoprecipitation assays indicated that HDAC7 directly binds with c-Myc gene and HDAC7 silencing decreased c-Myc mRNA level via reducing histone H3/H4 acetylation and repressing the association of RNA polymerase II (RNAP II) with c-Myc gene. Taken together, our findings highlight for the first time an unrecognized link between HDAC7 and c-Myc and offer a novel mechanistic insight into the contribution of HDAC7 to tumor progression.
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article, cas, google, scholar, pubmed, histone, hdac, cell, deacetylase, cmyc, cancer, expression, biol, mol, chen, gene, access, sci, usa, privacy, cookies, content, journal, research, regulation, apoptosis, senescence, nat, inhibitors, proc, natl, acad, myc, publish, search, proliferation, deacetylases, hdacs, silencing, activity, genes, proteins, marks, rev, dequiedt, class, chem, van, inhibitor, data,

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month download article/chapter jian ding & meiyu geng bypassing ras-induced senescence pbabe-puro-mycer plasmids histone deacetylase reveals hypoxia-inducible factor 1alpha c-myc/max dimerization cell cycle arrest suppressing c-myc expression cancer cells hdac7 silencing setting histone deacetylase inhibitors full article pdf privacy choices/manage cookies cancer cell lines c-myc gene usage analysis cancer cell proliferation innovation research group dna binding heterologous proteins rna polymerase ii signal pathway essential human leukemic lymphoblasts cdk inhibitor influences hdac7 directly binds check access knowledge innovation program instant access jian ding meiyu geng c-myc inactivation article zhu european economic area molecular medicine aims play fundamental roles chromatin immunoprecipitation assays related subjects single oncogenic lesion selective inhibition enhances oncogenic cooperation xiao-yong zhang state key laboratory electronic supplementary material histone deacetylases myc-regulated mirna conditions privacy policy cellular senescence article journal histone deacetylase 7

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         headline:The role of histone deacetylase 7 (HDAC7) in cancer cell proliferation: regulation on c-Myc
         description:Histone deacetylases (HDACs) play fundamental roles in the epigenetic regulation of gene expression and contribute to the growth, differentiation, and apoptosis of cancer cells. Although HDACs are recognized to be closely related to cancer development and altered expression of certain HDACs is observed in tumor samples, the arcane characters of HDACs in tumorigenesis have not been fully illustrated. Herein, we report that HDAC7 is a crucial player in cancer cell proliferation. Knockdown of HDAC7 resulted in significant G1/S arrest in different cancer cell lines. Subsequent investigations indicated that HDAC7 silencing blocked cell cycle progression through suppressing c-Myc expression and increasing p21 and p27 protein levels. The ectopic expression of c-Myc in turn antagonized the cell cycle arrest and repressed the elevation of p21 and p27 in HDAC7 silencing setting. Of note, HDAC7 deficiency was further identified to induce cellular senescence program, which was also reversed by c-Myc re-expression. Further chromatin immunoprecipitation assays indicated that HDAC7 directly binds with c-Myc gene and HDAC7 silencing decreased c-Myc mRNA level via reducing histone H3/H4 acetylation and repressing the association of RNA polymerase II (RNAP II) with c-Myc gene. Taken together, our findings highlight for the first time an unrecognized link between HDAC7 and c-Myc and offer a novel mechanistic insight into the contribution of HDAC7 to tumor progression.
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            Molecular Medicine
            Human Genetics
            Internal Medicine
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      description:Histone deacetylases (HDACs) play fundamental roles in the epigenetic regulation of gene expression and contribute to the growth, differentiation, and apoptosis of cancer cells. Although HDACs are recognized to be closely related to cancer development and altered expression of certain HDACs is observed in tumor samples, the arcane characters of HDACs in tumorigenesis have not been fully illustrated. Herein, we report that HDAC7 is a crucial player in cancer cell proliferation. Knockdown of HDAC7 resulted in significant G1/S arrest in different cancer cell lines. Subsequent investigations indicated that HDAC7 silencing blocked cell cycle progression through suppressing c-Myc expression and increasing p21 and p27 protein levels. The ectopic expression of c-Myc in turn antagonized the cell cycle arrest and repressed the elevation of p21 and p27 in HDAC7 silencing setting. Of note, HDAC7 deficiency was further identified to induce cellular senescence program, which was also reversed by c-Myc re-expression. Further chromatin immunoprecipitation assays indicated that HDAC7 directly binds with c-Myc gene and HDAC7 silencing decreased c-Myc mRNA level via reducing histone H3/H4 acetylation and repressing the association of RNA polymerase II (RNAP II) with c-Myc gene. Taken together, our findings highlight for the first time an unrecognized link between HDAC7 and c-Myc and offer a novel mechanistic insight into the contribution of HDAC7 to tumor progression.
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         c-Myc
         Cell cycle
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         Transcription
         Molecular Medicine
         Human Genetics
         Internal Medicine
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