HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer

Stojanović, Nataša; Hassan, Zonera; Wirth, Matthias; Wenzel, Patrick; Beyer, Mandy; Schäfer, Claudia; Brand, P. W. J. L.; Kroemer, Alexander; Stauber, Roland H.; Schmid, Roland M.; Arlt, Alexander; Sellmer, Andreas; Mahboobi, Siavosh; Rad, Roland; Reichert, Maximilian; Saur, Dieter; Krämer, Oliver; Schneider, Günter

doi:10.1038/onc.2016.344

Cited by 93 publications

(72 citation statements)

References 82 publications

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“…Previous studies suggested that upregulated MRGBP might promote proliferation of colorectal cancer cells through the regulation of BRD8 . Furthermore, MRGBP could regulate stability and/or synthesis of both TIP60/HAT complex and HDACs complexes, which are associated with tumor occurrence and advance, as well as aggressive biological behaviors . We previously revealed that MRGBP expression was significantly upregulated in PanCa samples and cell lines .…”

Section: Discussionmentioning

confidence: 94%

RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

Ding

Zhang

Gao

et al. 2018

J of Cellular Biochemistry

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miRNAs are small noncoding RNAs that act as critical epigenetic regulators in tumor carcinogenesis. In this study, our data showed that miR-137 was significantly downregulated in 58 pairs of human pancreatic cancer (PanCa) tissues and PanCa cell lines. Furthermore, the deregulated miR-137 was correlated with increased tumor size, higher TNM stage, and worse prognosis in pancreatic cancer. Functional studies demonstrated that overexpression of miR-137 dramatically suppressed cell proliferation and induced cell apoptosis in vitro. Meanwhile, upregulated miR-137 remarkably inhibited migration and invasion of pancreatic cancer cells. Further studies indicated that MRGBP was identified as the direct downstream target gene of miR-137. In addition, MRGBP expression is significantly downregulated in miR-137-transfected cells. Our previous study revealed that silencing of MRGBP suppressed the growth of PanCa cells in vitro and in vivo and also promoted apoptosis, and inhibited migration and invasion of PanCa cells, which are consistent with the effects of miR-137 overexpression. Taken together, our findings suggest that miR-137 may function as a novel tumor promoter through directly targeting MRGBP in PanCa.

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Section: Discussionmentioning

confidence: 94%

RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

Ding

Zhang

Gao

et al. 2018

J of Cellular Biochemistry

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“…It is clear that both histone acetylation and deacetylation affect chromatin remodeling as strong epigenetic mechanisms. Interestingly, evidence from several reports indicates that HDAC levels are increased in certain cancer types (22)(23)(24). In addition, HDAC inhibitors have been reported to enhance the acetylation of histones, in tumor cells (25).…”

Section: Hdac Inhibitors As Anti-cancer Agentsmentioning

confidence: 99%

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

2017

CGP

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“…HDAC inhibitors have a potent role in cancer pathogenesis and progression. A number of reports indicate that in certain types of cancer, HDAC levels are increased (21)(22)(23)(24).…”

Section: Hdac Inhibitors As Anti-breast Cancer Agentsmentioning

confidence: 99%

Histone Deacetylase Inhibitors: An Attractive Therapeutic Strategy Against Breast Cancer

et al. 2017

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Abstract. With a lifetime risk estimated to be one in eight in industrialized countriesBreast cancer is the most frequently diagnosed cancer and the second leading cause of cancer-related death among women worldwide. According to the American Cancer Society about 12% U.S. women will develop breast cancer during their lifetime. Moreover, in 2015, about 2,300 men were diagnosed with breast cancer and 440 died from the disease (1, 2).In approximately 90% of breast cancer cases, estrogen receptor α (ERα), progesterone receptor (PR), or the human epidermal growth factor receptor2 (HER2/ERBB2) protooncogenic receptor are expressed. In many of these patients, treatment with anti-estrogens (e.g. aromatase inhibitors, tamoxifen, fulvestrant) and HER2-targeted agents has improved their survival significantly (3, 4). However, despite 35

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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer

Cited by 93 publications

References 82 publications

RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

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

Histone Deacetylase Inhibitors: An Attractive Therapeutic Strategy Against Breast Cancer

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