HDAC2 promotes the EMT of colorectal cancer cells and via the modular scaffold function of ENSG00000274093.1

Qi, Zhipeng; Yalikong, Ayimukedisi; Zhang, Jia‐Wei; Cai, Shi‐Lun; Li, Bing; Sun, Da; Lv, Zhen-Tao; Xu, En‐Pan; Zhong, Yun‐Shi; Zhou, Ping‐Hong

doi:10.1111/jcmm.16186

Cited by 18 publications

(14 citation statements)

References 29 publications

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“…In line with our results, Li et al found that HDAC2 silencing evidently depressed cell proliferation and facilitated cell apoptosis in oesophageal squamous cell carcinoma EC9706 cells 15 . In addition, another research unveiled that HDAC2‐targeting shRNA caused suppression of the in vitro migration and invasion ability of colorectal cancer cells, which was concordant with our finding 16 . Also, ectopic expression of HDAC2 could lead to facilitation of the proliferation, migration and invasion of human trophoblast cells HTR‐8/SVNEO 17 …”

Section: Discussionsupporting

confidence: 93%

“…15 In addition, another research unveiled that HDAC2-targeting shRNA caused suppression of the in vitro migration and invasion ability of colorectal cancer cells, which was concordant with our finding. 16 Also, ectopic expression of HDAC2 could lead to facilitation of the proliferation, migration and invasion of human trophoblast cells HTR-8/SVNEO. 17 It has been widely recognized that HNF4A was a transcription factor to induce the expression of downstream factors.…”

Section: Discussionmentioning

confidence: 99%

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Histone deacetylase HDAC2 silencing prevents endometriosis by activating the HNF4A/ARID1A axis

Mai

Liao

Luo

et al. 2021

J Cellular Molecular Medi

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Histone deacetylase HDAC2 silencing prevents endometriosis by activating the HNF4A/ARID1A axis

Mai

Liao

Luo

et al. 2021

J Cellular Molecular Medi

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“…Benard et al found an increase in HDAC2 and a decrease in H3K56 acetylation in CRC tissues [ 36 ]. Qi and colleagues also reported that HDAC2 promotes EMT and metastasis in CRC cells by binding to a novel lncRNA [ 37 ]. HDACs are usually part of a multimeric co-repressive complex which is recruited to the E-cadherin promoter.…”

Section: Discussionmentioning

confidence: 99%

ZEB2/TWIST1/PRMT5/NuRD Multicomplex Contributes to the Epigenetic Regulation of EMT and Metastasis in Colorectal Carcinoma

Zheng

Dai

Yue

et al. 2022

Cancers

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(1) Background: The EMT plays a crucial role in tumor metastasis, which is the major cause for colorectal carcinoma-related mortality. However, the underlying regulators and mechanisms of EMT in CRC metastasis are still poorly understood; (2) Methods: The transcriptional regulators of EMT in CRC and their functions were examined using RT2212PCR, Western blotting, and luciferase reporter assay. The components of ZEB2/TWIST1 complex and their mutual interactions were identified via affinity purification, mass spectrometry, co-immunoprecipitation, and pull-down experiments. The functional mechanisms of ZEB2/TWIST1/PRMT5/NuRD axis were determined by chromatin immunoprecipitation and luciferase reporter assay. The contribution of ZEB2/TWIST1/PRMT5/NuRD complex in the CRC metastasis was investigated using wound healing, transwell assay, and in vivo xenograft mouse model; (3) Results: We found that ZEB2 and TWIST1 were both significantly upregulated in CRC tissues and EMT of CRC cells. ZEB2 could recruit TWIST1 to the E-cadherin promoter and synergistically repressed its transcription. In addition, ZEB2 physically interacted with TWIST1, PRMT5, and the nucleosome remodeling and deacetylase (NuRD) complex to form a novel repressive multicomplex, leading to epigenetic silencing of E-cadherin in CRC cells. Notably, the combined inhibition of ZEB2 and TWIST1 and epigenetic inhibition markedly reduced CRC metastasis in mice; (4) Conclusions: We revealed for the first time that ZEB2 could recruit TWIST1, PRMT5, and NuRD to form a repressive multicomplex and epigenetically suppresses the transcription of E-cadherin, thereby inducing the EMT process and metastasis in CRC. Our results also confirmed the therapeutic potential of epigenetic inhibitors in CRC.

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“…HDAC2 is a class I isoform of histone deacetylases, which could remove acetyl groups from histones, resulting in a tighter chromatin structure that regulates large amounts of gene transcription [30]. Previous studies shown that HDAC2 was upregulated in breast, colorectal and prostate cancers [31][32][33], and HDAC2 was associated with cancerpromoting molecular events. In addition, Lee et al pointed out that HDAC2/3 bound to acetylated BUB1B [34], leading to ubiquitin and degradation of BUB1B to participate in the cell mitosis process, which is consistent with our pathway analysis.…”

Section: Discussionmentioning

confidence: 99%

Clinical value and potential mechanisms of BUB1B up-regulation in nasopharyngeal carcinoma

Qin

Huang

et al. 2022

BMC Med Genomics

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Nasopharyngeal carcinoma (NPC) has insidious onset, late clinical diagnosis and high recurrence rate, which leads to poor quality of patient life. Therefore, it is necessary to further explore the pathogenesis and therapy targets of NPC. BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) was found to be up-regulated in a variety of cancers, but only two previous study showed that BUB1B was overexpressed in NPC and the sample size was small. The clinical role of BUB1B expression and its underlying mechanism in NPC require more in-depth research. Immunohistochemical samples and public RNA-seq data indicated that BUB1B protein and mRNA expression levels were up-regulated in NPC, and summary receiver operating characteristic curve indicated that BUB1B expression level had a strong ability to distinguish NPC tissues from non-NPC tissues. Gene ontology and Kyoto Encyclopedia of genes and genomes were performed and revealed that BUB1B and its related genes were mainly involved in cell cycle and DNA replication. Protein- Protein Interaction were built to interpret the BUB1B molecular mechanism. Histone deacetylase 2 (HDAC2) could be the upstream regulation factor of BUB1B, which was verified by Chromatin Immunoprecipitation Sequencing samples. In summary, BUB1B was highly expressed in NPC, and HDAC2 may affect cell cycle by regulating BUB1B to promote cancer progression.

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HDAC2 promotes the EMT of colorectal cancer cells and via the modular scaffold function of ENSG00000274093.1

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 18 publications

References 29 publications

Histone deacetylase HDAC2 silencing prevents endometriosis by activating the HNF4A/ARID1A axis

Histone deacetylase HDAC2 silencing prevents endometriosis by activating the HNF4A/ARID1A axis

ZEB2/TWIST1/PRMT5/NuRD Multicomplex Contributes to the Epigenetic Regulation of EMT and Metastasis in Colorectal Carcinoma

Clinical value and potential mechanisms of BUB1B up-regulation in nasopharyngeal carcinoma

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