We are analyzing https://link.springer.com/article/10.1186/s12943-017-0736-2.

Title:
Hdac7 promotes lung tumorigenesis by inhibiting Stat3 activation | Molecular Cancer
Description:
Background Lung cancer is the leading cause of cancer death worldwide. However, the molecular mechanisms underlying lung cancer development have not been fully understood. The functions of histone deacetylases (HDACs), a class of total eighteen proteins (HDAC1–11 and SIRT1–7 in mammals) that deacetylate histones and non-histone proteins, in cancers are largely unknown. Methods Hdac7 +/−/K-Ras mice and HDAC7-depleted human lung cancer cell lines were used as models for studying the function of Hdac7 gene in lung cancer. Kaplan-Meier survival analysis was performed to explore the relationship between HDAC7 expression and prognosis of human lung cancers. Recombinant lentivirus-mediated in vivo gene expression or knockdown, Western blotting, and pull-down assay were applied to investigate the underlying molecular mechanism by which Hdac7 promotes lung tumorigenesis. Results The number and burden of lung tumor were dramatically reduced in Hdac7 +/−/K-Ras mice compared to control K-Ras mice. Also, in Hdac7 +/−/K-Ras mice, cell proliferation was significantly inhibited and apoptosis in lung tumors was greatly enhanced. Similarly, cell proliferation and anchorage-independent growth of human lung cancer cell lines expressing shHDAC7 were also significantly suppressed and apoptosis was dramatically elevated respectively. Mechanistic study revealed that Hdac7 mutation in mouse lung tumors or HDAC7 depletion in human tumor cell lines resulted in significantly enhanced acetylation and tyrosine-phosphorylation of Stat3 and HDAC7 protein directly interacted with and deacetylateed STAT3. The Hdac7 mutant-mediated inhibitory effects on lung tumorigenesis in mice and cell proliferation/soft agar colony formation of human lung cancer cell lines were respectively reversed by expressing dnStat3. Finally, the high HDAC7 mRNA level was found to be correlated with poor prognosis of human lung cancer patients. Conclusion Our study suggests that Hdac7 promotes lung tumorigenesis by inhibiting Stat3 activation via deacetylating Stat3 and may shed a light on the design of new therapeutic strategies for human lung cancer.
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hdac, lung, cancer, stat, mice, human, cells, pubmed, tumor, expression, article, kras, cell, google, scholar, cas, tumors, fig, mouse, phosphorylation, protein, assay, results, control, deacetylase, analysis, prognosis, proliferation, histone, proteins, apoptosis, growth, central, acetylation, level, tumorigenesis, mutant, function, class, lines, activity, development, western, expressing, patients, blot, significantly, panel, cancers, shhdac,

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sex-specific genomic profiles lsl-k-ras g12d allele lenti-cre-2a-dnstat3 infected group lsl-k-ras g12d mice real-time qrt-pcr results lenti-cre-2a-dnstat3 viruses plasmid pfuw-cre-2a-dnstat3 human cancer cell lines pan anti-acetyl-lysine antibodies class iia-specific substrates article download pdf kaplan-meier survival analysis randomly chosen fields/lung shicheng guo hdac7-depleted h1299 cells lenti-cre infected group k-ras transgenic mice dna binding/promoter occupation called k-ras mice hdac7 +/−/k-ras mice lenti-cre-2a-dnstat3 tumor-suppressor gene promoters arhi tumor-suppressor gene affinity purified gst-hdac7 gst-hdac7 fusion protein open research fund control k-ras mice flag-tagged stat3 protein histone acetyl transferases/hdacs national key research flag-tagged stat3 proteins histone deacetylase reveals lenti-cre expressing cre growth suppression mediated ip-western blot analysis anti-acetylated lysine antibody plasmid pcmv6-stat3-flag state key laboratory mutant k-ras providing plasmids pmx-stat3 high py-stat3 level human lung cancer suppresses cancer proliferation hdac7-depletion inhibited angiogenesis full access hdac7-depleted h1299 histone deacetylase inhibition human cancer cells glutathione s-transferase squamous cell carcinoma

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HDAC family: what are the cancer relevant targets?

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         description:Lung cancer is the leading cause of cancer death worldwide. However, the molecular mechanisms underlying lung cancer development have not been fully understood. The functions of histone deacetylases (HDACs), a class of total eighteen proteins (HDAC1–11 and SIRT1–7 in mammals) that deacetylate histones and non-histone proteins, in cancers are largely unknown. Hdac7 +/−/K-Ras mice and HDAC7-depleted human lung cancer cell lines were used as models for studying the function of Hdac7 gene in lung cancer. Kaplan-Meier survival analysis was performed to explore the relationship between HDAC7 expression and prognosis of human lung cancers. Recombinant lentivirus-mediated in vivo gene expression or knockdown, Western blotting, and pull-down assay were applied to investigate the underlying molecular mechanism by which Hdac7 promotes lung tumorigenesis. The number and burden of lung tumor were dramatically reduced in Hdac7 +/−/K-Ras mice compared to control K-Ras mice. Also, in Hdac7 +/−/K-Ras mice, cell proliferation was significantly inhibited and apoptosis in lung tumors was greatly enhanced. Similarly, cell proliferation and anchorage-independent growth of human lung cancer cell lines expressing shHDAC7 were also significantly suppressed and apoptosis was dramatically elevated respectively. Mechanistic study revealed that Hdac7 mutation in mouse lung tumors or HDAC7 depletion in human tumor cell lines resulted in significantly enhanced acetylation and tyrosine-phosphorylation of Stat3 and HDAC7 protein directly interacted with and deacetylateed STAT3. The Hdac7 mutant-mediated inhibitory effects on lung tumorigenesis in mice and cell proliferation/soft agar colony formation of human lung cancer cell lines were respectively reversed by expressing dnStat3. Finally, the high HDAC7 mRNA level was found to be correlated with poor prognosis of human lung cancer patients. Our study suggests that Hdac7 promotes lung tumorigenesis by inhibiting Stat3 activation via deacetylating Stat3 and may shed a light on the design of new therapeutic strategies for human lung cancer.
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          Stat3
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            name:MOE Key Laboratory of Contemporary Anthropology and Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University
            address:
               name:MOE Key Laboratory of Contemporary Anthropology and Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Bo Su
      affiliation:
            name:Shanghai Pulmonary Hospital, Tongji University
            address:
               name:Shanghai Pulmonary Hospital, Tongji University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Yuchao Fang
      affiliation:
            name:Huashan Hospital, Fudan University
            address:
               name:Huashan Hospital, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Xiaofeng Chen
      affiliation:
            name:Huashan Hospital, Fudan University
            address:
               name:Huashan Hospital, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Hengning Ke
      affiliation:
            name:Cancer Research Institute, General Hospital, Ningxia Medical University
            address:
               name:Cancer Research Institute, General Hospital, Ningxia Medical University, Yinchuan, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Wufan Tao
      affiliation:
            name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University
            address:
               name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
            name:Cancer Research Institute, General Hospital, Ningxia Medical University
            address:
               name:Cancer Research Institute, General Hospital, Ningxia Medical University, Yinchuan, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:MOE Key Laboratory of Contemporary Anthropology and Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:MOE Key Laboratory of Contemporary Anthropology and Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:Shanghai Pulmonary Hospital, Tongji University, Shanghai, China
      name:Huashan Hospital, Fudan University, Shanghai, China
      name:Huashan Hospital, Fudan University, Shanghai, China
      name:Cancer Research Institute, General Hospital, Ningxia Medical University, Yinchuan, China
      name:Obstetrics & Gynecology Hospital and State Key Laboratory of Genetic Engineering and Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China
      name:Cancer Research Institute, General Hospital, Ningxia Medical University, Yinchuan, China

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