HDAC1 promoted migration and invasion binding with TCF12 by promoting EMT progress in gallbladder cancer

He, Junyi; Shen, Sheng; Lu, Weiqi; Zhou, Yuhong; Hou, Yingyong; Zhang, Yong; Jiang, Ying; Liu, Houbao; Shao, Yijia

doi:10.18632/oncotarget.8740

Cited by 33 publications

(38 citation statements)

References 31 publications

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“…Identification of the key mechanism underlying GC is imperative. In previous studies, TCF12 has been shown to play a key role in the diversity of human cancers . We thus investigate whether TCF12 was differentially expressed in GC tissues.…”

Section: Discussionmentioning

confidence: 96%

Retracted: High expression of TCF12 contributes to gastric cancer development via being target regulated by miR‐183 and activating PI3K/AKT pathway

Wang

Gao

Xie

et al. 2019

J of Cellular Biochemistry

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This study aimed to explore the role of transcription factor 12 (TCF12) in the process of gastric cancer (GC) and to elucidate its possible regulatory mechanism. The expression data of GC tissues and matched normal tissues were downloaded from The Cancer Genome Atlas (TCGA) database. Survival analysis for GC patients with different levels of TCF12 was performed by the Kaplan-Meier analysis. In addition, TCF12 was suppressed in human GC cell lines AGS and MKN-45, followed by detecting cell biological processes (proliferation, apoptosis, migration, and invasion). Moreover, the association between TCF12 and the phosphatidylinositol 3-kinase (PI3K)/AKT signal was elucidated. Besides, the potential micro RNAs that could target TCF12 expression were explored. The results showed that TCF12 was highly expressed in GC tissues and TCF12 upregulation was associated with poor prognosis of GC patients. In addition, suppression of TCF12 significantly inhibited the proliferation, migration, and invasion of both AGS and MKN45 cells, as well as induced apoptosis of the two cell lines. Moreover, suppression of TCF12 significantly decreased the expression of p-AKT, cyclin D1, p-P70, and β-catenin in both AGS and MKN45 cells. Besides, TCF12 was target regulated by miR-183 in GC cells. Our findings reveal that TCF12 is upregulated in GC and its upregulation is associated with poor prognosis of GC patients. To sum up, downregulation of TCF12 may inhibit GC development via being target regulated by miR-183 and inhibiting the PI3K/AKT signal. TCF12 may function as a potential therapeutic target for GC.

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Section: Discussionmentioning

confidence: 96%

Retracted: High expression of TCF12 contributes to gastric cancer development via being target regulated by miR‐183 and activating PI3K/AKT pathway

Wang

Gao

Xie

et al. 2019

J of Cellular Biochemistry

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“…A global H3K27 deacetylation was also observed, suggesting it is a key epigenetic event in ZEB1-induced transcriptional reprogramming [86]. In addition to EMT-TFs, HDAC1 is co-purified with TCF12 while the elevated expression of TCF12 and HDAC1 correlates with poor prognosis of gallbladder cancer patients [87], indicating that this HLH transcription factor could also targets HDACs for epithelial gene silencing during EMT. Intriguingly, HDAC6 and SIRT1 have been shown to counteract p300-catalyzed acetylation on Cortactin and thus enhance its F-actin binding ability to facilitate EMT and tumor progression [88,89].…”

Section: Permissive Histone Modifications In Emtmentioning

confidence: 99%

Epigenetic regulation of epithelial–mesenchymal transition

Sun

Fang

2016

Cell. Mol. Life Sci.

108

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Epithelial-mesenchymal transition (EMT) is an essential process for morphogenesis and organ development which reversibly enables polarized epithelial cells to lose their epithelial characteristics and acquire mesenchymal properties. It is now evident that the aberrant activation of EMT is also a critical mechanism to endow epithelial cancer cells with migratory and invasive capabilities associated with metastatic competence. This dedifferentiation program is mediated by a small cohort of pleiotropic transcription factors which in turn orchestrate a complex array of epigenetic mechanisms for the widespread changes in gene expression. Here, we review major epigenetic mechanisms with emphasis on histone modifications and discuss their implications in EMT and tumor progression. We also highlight mechanisms underlying transcription regulation concerted by various chromatin modifying proteins and EMT-inducing transcription factors at different molecular layers. Owing to the reversible nature of epigenetic modifications, a thorough understanding of their functions in EMT will not only provide new insights into our knowledge of cancer progression and metastasis, but also facilitates the development of diagnostic and therapeutic strategies for human malignancy.

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“…Epithelial-mesenchymal transition (EMT), several oncogenic cues have been suggested could increase GBC cells growth and stemness through promoting EMT process [14, 15]. Hypoxia-inducible factor-1α subunit (HIF-1α), a key factor in resisting oxidative stress, could also promote aggressive phenotype of cancer cells through different types of intracellular signal transduction pathways, including EMT activation [16-22].…”

Section: Introductionmentioning

confidence: 99%

MiR-143-5p Deficiency Triggers EMT and Metastasis by Targeting HIF-1α in Gallbladder Cancer

He¹,

Zhan²,

Chen³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Early metastasis plays a pivotal role in tumor-caused death in gallbladder cancer (GBC) patients. Increasing evidence suggest that miR-143-5p is an active player involved in cancer metastasis and a potential therapeutic target. However, its role in the development of GBC cells remains unclear. The aim of this study is to reveal the inhibiting effects of miR-143-5p on the proliferation and metastasis in GBC. Methods: Quantitative real-time PCR were used to investigate miR-143-5p and its target HIF-1α mRNA levels. Protein expression was measured by immunohistochemistry and western blot. The function and regulation mechanism of miR-143-5p was confirmed by MTS, colony formation, wound healing, transwell, and luciferase reporter assays. Results: miR-143-5p was first found significantly reduced in GBC tissues compared with corresponding noncancerous gallbladder tissues. In addition, miR-143-5p deficiency correlated well with larger tumor size, advanced TNM stage, and poorer survival rate. In vitro, miR-143-5p addition dramatically suppressed GBC cells proliferation, migration and invasion, whereas miR-143-5p antisense led the opposite effects. Further elucidating the molecular mechanism inside, we found miR-143-5p exerted its inhibitory function through downregulating the expression of HIF-1α, which further reduced Twist1 and impeded epithelial-mesenchymal transition (EMT). Conclusions: Altogether, our studies identified a novel regulator, miR-143-5p, implicated in GBC prognosis through targeting HIF-1α/EMT related signaling pathway, which could serve as a biomarker and therapeutic target for GBC.

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HDAC1 promoted migration and invasion binding with TCF12 by promoting EMT progress in gallbladder cancer

Cited by 33 publications

References 31 publications

Retracted: High expression of TCF12 contributes to gastric cancer development via being target regulated by miR‐183 and activating PI3K/AKT pathway

Retracted: High expression of TCF12 contributes to gastric cancer development via being target regulated by miR‐183 and activating PI3K/AKT pathway

Epigenetic regulation of epithelial–mesenchymal transition

MiR-143-5p Deficiency Triggers EMT and Metastasis by Targeting HIF-1α in Gallbladder Cancer

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