Dataset Information

NR1D2 Accelerates Hepatocellular Carcinoma Progression by Driving the Epithelial-to-Mesenchymal Transition.

ABSTRACT: Introduction:A poor prognosis owing to cancer invasion and metastasis, hepatocellular carcinoma (HCC) is one of the leading causes of malignancy deaths worldwide. A dominant epithelial-to-mesenchymal transition or EMT function in tumour metastasis is substantially evidenced. Prior reports identified a likely correlation of the nuclear hormone receptor NR1D2 with HCC progression, but the underlying molecular mechanisms and role of invasion and metastasis are still to be adequately documented. Methods:We carried out PROGgeneV2 platform database analysis and compared NR1D2 expression in HCC tissues with that in adjacent noncancerous tissues by Western blotting. Cell proliferation, invasion, and migration were also assessed using a lentivirus system. Moreover, the relevant signalling proteins were evaluated. Results:The PROGgeneV2 platform database analysis suggested an upregulated NR1D2 expression related to poor overall survival, or OS, in HCC, with higher levels in HCC, compared to the adjoining non-cancerous tissue. Depleting NR1D2 decreased HCC cell proliferation, migration and invasion in vitro, whilst in vivo downregulation revealed fewer metastatic nodules in the lungs. Furthermore, NR1D2 knockdown amplified epithelial marker, namely E-cadherin expressions, and decreased mesenchymal markers, ie, N-cadherin and vimentin expressions, with ?-catenin overexpression. Conclusion:NR1D2 is shown to accelerate HCC progression via driving EMT.

SUBMITTER: Tong H

PROVIDER: S-EPMC7217318 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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<i>NR1D2</i> Accelerates Hepatocellular Carcinoma Progression by Driving the Epithelial-to-Mesenchymal Transition.

Tong Hui H Liu Xiaohui X Li Tao T Qiu Weihua W Peng Chenghong C Shen Baiyong B Zhu Zhecheng Z

OncoTargets and therapy 20200508

<h4>Introduction</h4>A poor prognosis owing to cancer invasion and metastasis, hepatocellular carcinoma (HCC) is one of the leading causes of malignancy deaths worldwide. A dominant epithelial-to-mesenchymal transition or EMT function in tumour metastasis is substantially evidenced. Prior reports identified a likely correlation of the nuclear hormone receptor <i>NR1D2</i> with HCC progression, but the underlying molecular mechanisms and role of invasion and metastasis are still to be adequately ...[more]

PMID: 32440156

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Project description:Negative elongation factor-B (NELF-B), also known as cofactor of BRCA1 (COBRA1), is one of the four subunits of the NELF complex. It interacts with BRCA1, in addition to other transcription complexes in various tissues. The NELF complex represses the transcription of several genes by stalling RNA polymerase II during the early phase of transcription elongation. The role of NELF-B in liver cancer and hepatocellular carcinoma (HCC), the most prevalent type of liver cancer, remains to be elucidated. It has been previously demonstrated that silencing of NELF-B inhibits the proliferation and migration of HepG2 cells. The present study aimed to investigate the consequences of ectopic expression and silencing of NELF-B in liver cancer HepG2 and SNU449 cell lines. Functional assays were performed to examine the effects on gene and protein expression, viability, migration and invasion of cells. Overexpression of NELF-B did not alter the proliferation and migration of HepG2 cells, or the expression of tested genes, indicating that overexpression alone may not be sufficient for altering these features in HepG2 cells. By contrast, knockdown of NELF-B in SNU449 cells resulted in decreased cell proliferation, together with induction of apoptosis and decreased expression levels of Ki-67 and survivin, which are markers of proliferation and inhibition of apoptosis, respectively. Additionally, silencing of NELF-B resulted in a significant decrease in the hallmarks of epithelial-mesenchymal transition (EMT), including cell migration and invasion, and decreased the expression levels of EMT markers, such as N-cadherin, vimentin and β-catenin. Decreased expression levels of forkhead box F2 transcription factor and increased mRNA levels of trefoil factor 1, a putative tumor suppressor, were also detected following the silencing of NELF-B. The current results demonstrated that NELF-B enhanced the manifestation of most hallmarks of cancer, including cell proliferation, migration, invasion and inhibition of apoptosis, indicating its critical role in the progression of HCC.

Dataset Information

NR1D2 Accelerates Hepatocellular Carcinoma Progression by Driving the Epithelial-to-Mesenchymal Transition.

Publications

<i>NR1D2</i> Accelerates Hepatocellular Carcinoma Progression by Driving the Epithelial-to-Mesenchymal Transition.

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