组蛋白脱乙酰基酶作为三阴性乳腺癌的新治疗靶点：进展和承诺。,Cancer Genomics & Proteomics

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组蛋白脱乙酰基酶作为三阴性乳腺癌的新治疗靶点：进展和承诺。
Cancer Genomics & Proteomics ( IF 2.6 ) Pub Date : 2017-09-06 , DOI: 10.21873/cgp.20041
Nikolaos Garmpis ₁ , Christos Damaskos _{2,

3} , Anna Garmpi ₄ , Emmanouil Kalampokas ₅ , Theodoros Kalampokas ₆ , Eleftherios Spartalis ₃ , Afrodite Daskalopoulou ₃ , Serena Valsami ₇ , Michael Kontos ₈ , Afroditi Nonni ₉ , Konstantinos Kontzoglou ₂ , Despina Perrea ₃ , Nikolaos Nikiteas ₃ , Dimitrios Dimitroulis ₂

Affiliation

Second Department of Propedeutic Surgery, Laiko General Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece
Second Department of Propedeutic Surgery, Laiko General Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece.
N.S. Christeas Laboratory of Experimental Surgery and Surgical Research, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Internal Medicine Department, Laiko General Hospital, University of Athens Medical School, Athens, Greece.
Gynaecological Oncology Department, University of Aberdeen, Aberdeen, U.K.
Assisted Conception Unit, Second Department of Obstetrics and Gynecology, Aretaieion Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Blood Transfusion Department, Aretaieion Hospital, Medical School, National and Kapodistrian Athens University, Athens, Greece.
First Department of Surgery, Laiko General Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
First Department of Pathology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.

三阴性乳腺癌（TNBC）缺乏雌激素受体（ER），孕激素受体（PR）和HER2基因的表达。它包含约15-20％的乳腺癌（BCs）。不幸的是，TNBC的治疗由于其相对较差的预后，侵略性和缺乏针对性疗法而仍然是临床问题，使化学疗法成为治疗的主要手段。找到新的针对TNBC的疗法至关重要，以超越现有疗法的耐药性和侵袭性。考虑到表观遗传过程控制着TNBC的启动和发展这一事实，人们越来越关注参与致癌基因表达的表观遗传调控的机制，分子和信号传导途径。组蛋白的乙酰化激发了涉及细胞生长的基因的转录，并且在许多恶性肿瘤中，组蛋白脱乙酰基酶（HDACs）的表达经常被上调。不幸的是，在BC领域，HDAC抑制剂作为单药显示有限的作用。尽管如此，目前正在评估它们与激酶抑制剂，自噬抑制剂，电离辐射或两种HDAC抑制剂一起使用的情况。HDAC抑制剂，如亚磺酰苯胺异羟肟酸（SAHA），丁酸钠，mocetinostat，panobinostat，entinostat，YCW1和N-（2-羟苯基）-2-丙基戊酰胺对TNBC表现出良好的治疗效果，尤其是与其他抗癌药联合使用时代理商。

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Histone Deacetylases as New Therapeutic Targets in Triple-negative Breast Cancer: Progress and Promises.

Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR) and HER2 gene. It comprises approximately 15-20% of breast cancers (BCs). Unfortunately, TNBC's treatment continues to be a clinical problem because of its relatively poor prognosis, its aggressiveness and the lack of targeted therapies, leaving chemotherapy as the mainstay of treatment. It is essential to find new therapies against TNBC, in order to surpass the resistance and the invasiveness of already existing therapies. Given the fact that epigenetic processes control both the initiation and progression of TNBC, there is an increasing interest in the mechanisms, molecules and signaling pathways that participate at the epigenetic modulation of genes expressed in carcinogenesis. The acetylation of histone proteins provokes the transcription of genes involved in cell growth, and the expression of histone deacetylases (HDACs) is frequently up-regulated in many malignancies. Unfortunately, in the field of BC, HDAC inhibitors have shown limited effect as single agents. Nevertheless, their use in combination with kinase inhibitors, autophagy inhibitors, ionizing radiation, or two HDAC inhibitors together is currently being evaluated. HDAC inhibitors such as suberoylanilidehydroxamic acid (SAHA), sodium butyrate, mocetinostat, panobinostat, entinostat, YCW1 and N-(2-hydroxyphenyl)-2-propylpentanamide have shown promising therapeutic outcomes against TNBC, especially when they are used in combination with other anticancer agents. More studies concerning HDAC inhibitors in breast carcinomas along with a more accurate understanding of the TNBC's pathobiology are required for the possible identification of new therapeutic strategies.

更新日期：2019-11-01

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