Emerging Roles of Epigenetic Regulator Sin3 in Cancer

被引：47

作者：

Bansal, N. ^{[1
]}

David, G. ^{[2
]}

Farias, E. ^{[1
]}

Waxman, S. ^{[1
]}

机构：

[1] Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA

[2] NYU, Sch Med, New York, NY USA

来源：

ADVANCES IN CANCER RESEARCH, VOL 130 | 2016年 / 130卷

关键词：

HISTONE DEACETYLASE COMPLEX; NEGATIVE BREAST-CANCER; TRANSCRIPTIONAL REPRESSION; METASTASIS SUPPRESSOR-1; CELLULAR SENESCENCE; WILD-TYPE; COREPRESSOR; CELLS; MYC; INTERACTS;

D O I：

10.1016/bs.acr.2016.01.006

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Revolutionizing treatment strategies is an urgent clinical need in the fight against cancer. Recently the scientific community has recognized chromatin-associated proteins as promising therapeutic candidates. However, there is a need to develop more targeted epigenetic inhibitors with less toxicity. Sin3 family is one such target which consists of evolutionary conserved proteins with two paralogues Sin3A and Sin3B. Sin3A/B are global transcription regulators that provide a versatile platform for diverse chromatin-modifying activities. Sin3 proteins regulate key cellular functions that include cell cycle, proliferation, and differentiation, and have recently been implicated in cancer pathogenesis. In this chapter, we summarize the key concepts of Sin3 biology and elaborate the recent advancements in the role of Sin3 proteins in cancer with specific examples in multiple endocrine neoplasia type 2, pancreatic ductal adenocarcinoma, and triple negative breast cancer. Finally, a program to create an integrative approach for screening antitumor agents that target chromatin-associated factors like Sin3 is presented.

引用

页码：113 / 135

页数：23

共 79 条

[1]

Molecular heterogeneity of triple-negative breast cancer [J].

Abramson V.G. ;

Mayer I.A. .

Current Breast Cancer Reports, 2014, 6 (3) :154-158

[2]

Optimal strategies for the treatment of metastatic triple-negative breast cancer with currently approved agents [J].

Andre, F. ;

Zielinski, C. C. .

ANNALS OF ONCOLOGY, 2012, 23 :46-51

[3]

[Anonymous], 2015, CANC FACTS FIG 2015

[4]

Ayer DE, 1996, MOL CELL BIOL, V16, P5772

[5]

A Positive Regulatory Role for the mSin3A-HDAC Complex in Pluripotency through Nanog and Sox2 [J].

Baltus, Gretchen A. ;

Kowalski, Michael P. ;

Tutter, Antonin V. ;

Kadam, Shilpa .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (11) :6998-7006

[6]

Targeting the SIN3A-PF1 interaction inhibits epithelial to mesenchymal transition and maintenance of a stem cell phenotype in triple negative breast cancer [J].

Bansal, Nidhi ;

Petrie, Kevin ;

Christova, Rossitza ;

Chung, Chi-Yeh ;

Leibovitch, Boris A. ;

Howell, Louise ;

Gil, Veronica ;

Sbirkov, Yordan ;

Lee, EunJee ;

Wexler, Joanna ;

Ariztia, Edgardo V. ;

Sharma, Rajal ;

Zhu, Jun ;

Bernstein, Emily ;

Zhou, Ming-Ming ;

Zelent, Arthur ;

Farias, Eduardo ;

Waxman, Samuel .

ONCOTARGET, 2015, 6 (33) :34087-34105

[7]

Tumor Suppressor Protein p53 Recruits Human Sin3B/HDAC1 Complex for Down-Regulation of Its Target Promoters in Response to Genotoxic Stress [J].

Bansal, Nidhi ;

Kadamb, Rama ;

Mittal, Shilpi ;

Vig, Leena ;

Sharma, Raisha ;

Dwarakanath, Bilikere S. ;

Saluja, Daman .

PLOS ONE, 2011, 6 (10)

[8]

Perspective on unraveling the versatility of 'co-repressor' complexes [J].

Baymaz, H. Irem ;

Karemaker, Ino D. ;

Vermeulen, Michiel .

BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS, 2015, 1849 (08) :1051-1056

[9]

From single cells to deep phenotypes in cancer [J].

Bendall, Sean C. ;

Nolan, Garry P. .

NATURE BIOTECHNOLOGY, 2012, 30 (07) :639-647

[10]

REARRANGEMENTS OF THE RETINOIC ACID RECEPTOR-ALPHA AND PROMYELOCYTIC LEUKEMIA ZINC-FINGER GENES RESULTING FROM T(11 17)(Q23 Q21) IN A PATIENT WITH ACUTE PROMYELOCYTIC LEUKEMIA [J].

CHEN, SJ ;

ZELENT, A ;

TONG, JH ;

YU, HQ ;

WANG, ZY ;

DERRE, J ;

BERGER, R ;

WAXMAN, S ;

CHEN, Z .

JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (05) :2260-2267

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