Basic Transcription Factor 3 Is Required for Proliferation and Epithelial‐Mesenchymal Transition via Regulation of FOXM1 and JAK2/STAT3 Signaling in Gastric Cancer

Zhang, Dezhong; Chen, Binghe; Zhang, Lanfang; Cheng, Mingkun; Fang, Xiangjie; Wu, Ximei

doi:10.3727/096504017x14886494526344

Cited by 22 publications

(15 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Here, we show that the transcription factor BTF3 binds to the promoter region of n-cadherin 41 with the help of Cx43 and together positively regulate n-cadherin expression. Thus, BTF3, a transcription factor previously associated with gene expression in cancer systems 20 , 21 , regulates embryonic gene expression in neural crest, a cell population that has been likened to cancer cells 42 . Cx43 has been postulated to be upregulated in later stages of neural crest development 40 as in several cancer systems 43 , 44 , in order to modulate cell migration.…”

Section: Discussionmentioning

confidence: 99%

“…BTF3 is able to form a stable complex with polymerase II and is part of the transcription initiation complex 17 , 18 . In more recent studies, BTF3 upregulation has been correlated with tumor prognosis 19 , 20 and the transcriptional activity of BTF3 has been implicated in proliferation and cancer progression 20 , 21 . Here, we demonstrate that Cx43-tail, BTF3 and Pol II altogether form a complex that directly binds to the n-cad promoter to modulate N-cadherin transcription.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

et al. 2018

View full text Add to dashboard Cite

Connexins are the primary components of gap junctions, providing direct links between cells under many physiological processes. Here, we demonstrate that in addition to this canonical role, Connexins act as transcriptional regulators. We show that Connexin 43 (Cx43) controls neural crest cell migration in vivo by directly regulating N-cadherin transcription. This activity requires interaction between Cx43 carboxy tail and the basic transcription factor-3, which drives the translocation of Cx43 tail to the nucleus. Once in the nucleus they form a complex with PolII which directly binds to the N-cadherin promoter. We found that this mechanism is conserved between amphibian and mammalian cells. Given the strong evolutionary conservation of connexins across vertebrates, this may reflect a common mechanism of gene regulation by a protein whose function was previously ascribed only to gap junctional communication.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The 5 genes have been demonstrated to be related to lung cancer and some other kinds of cancers by experimental approaches in previous literatures. Specifically, BTF3 was confirmed aberrantly in various cancer tissues such as gastric cancer tissues [47,48], prostate cancer tissues [49], colorectal cancer tissues [50] and pancreatic cancer cells [51]; RPS16 was found dysregulated in disc degeneration, which is one of the main causes of low back pain [52]; HSF1 influenced the expression of heat shock proteins as well as other activities like the induction of tumor suppressor genes, signal transduction pathway, and glucose metabolism. Its associations with gastric cancer [53], breast cancer and two of the studied SNPs correlated significantly with cancer development [54] have been proved; RPS6 was declared closely relevant to the nonsmall cell lung cancer (NSCLC) [55], the renal cell carcinoma [56] and some other cancers [57,58]; MAPKAPK2 was demonstrated to contribute to tumor progression by promoting M2 macrophage polarization and tumor angiogenesis [59].…”

Section: Discussionmentioning

confidence: 99%

Bayesian differential analysis of gene regulatory networks exploiting genetic perturbations

Liu

et al. 2020

BMC Bioinformatics

View full text Add to dashboard Cite

Background: Gene regulatory networks (GRNs) can be inferred from both gene expression data and genetic perturbations. Under different conditions, the gene data of the same gene set may be different from each other, which results in different GRNs. Detecting structural difference between GRNs under different conditions is of great significance for understanding gene functions and biological mechanisms. Results: In this paper, we propose a Bayesian Fused algorithm to jointly infer differential structures of GRNs under two different conditions. The algorithm is developed for GRNs modeled with structural equation models (SEMs), which makes it possible to incorporate genetic perturbations into models to improve the inference accuracy, so we name it BFDSEM. Different from the naive approaches that separately infer pair-wise GRNs and identify the difference from the inferred GRNs, we first re-parameterize the two SEMs to form an integrated model that takes full advantage of the two groups of gene data, and then solve the re-parameterized model by developing a novel Bayesian fused prior following the criterion that separate GRNs and differential GRN are both sparse. Conclusions: Computer simulations are run on synthetic data to compare BFDSEM to two state-of-the-art joint inference algorithms: FSSEM and ReDNet. The results demonstrate that the performance of BFDSEM is comparable to FSSEM, and is generally better than ReDNet. The BFDSEM algorithm is also applied to a real data set of lung cancer and adjacent normal tissues, the yielded normal GRN and differential GRN are consistent with the reported results in previous literatures. An open-source program implementing BFDSEM is freely available in Additional file 1.

show abstract

“…Activation of JAK2 protein kinase can catalyze STAT3 protein phosphorylation which regulates the expression of oncogenic genes [23]. E-cadherin, Ncadherin and ZEB2 are well-known downstream molecules of JAK2/STAT3 signalling pathway [24][25][26].…”

Section: Discussionmentioning

confidence: 99%

CCL18-NIR1/GPR3 promotes oral cancer cell growth and metastasis by activating the JAK2/STAT3 signalling pathway

Chen

Jiang

Sun

et al. 2019

Preprint

View full text Add to dashboard Cite

Background Chemokine (C-C motif) ligand 18 (CCL18) affects the malignant progression of varying cancers by activating chemokine receptors. Our previous study have shown that CCL18 promotes hyperplasia and invasiveness of oral cancer cells; however, the cognate receptors of CCL18 involved in the pathogenesis of oral squamous cell carcinoma (OSCC) has not yet been identified. This study aimed to investigate the underlying molecular mechanisms through which CCL18 promotes OSCC progression by binding to specific functional receptors.Methods The properties of CCL18 receptors (i.e., NIR1, CCR6, CCR8, and GPR3) in OSCC were detected by conducting western blotting, immunofluorescence, and immunocytochemistry assays. The binding between CCL18 and its receptors was verified by performing coimmunoprecipitation (CO-IP) assays. The χ2 test was applied to analyze the relationship between CCL18 receptor expression patterns and clinicopathological factors. Recombinant CCL18 (rCCL18) and receptor siRNA were used to confirm the effects of CCL18 receptor axis on the morphology of cancer cells (i.e., proliferation, and metastasis), epithelial-mesenchymal transition (EMT) and the expression of the JAK2/STAT3 signalling pathway.Results NIR1 and GPR3 as specific receptors of CCL18 in OSCC were found to be significantly increased and positively related to the TNM stage of OSCC patients. rCCL18 induced phenotype alterations of oral cancer cells including cell growth, metastasis, and EMT. Knockdown of NIR1 and/or GPR3 expression could block the effects of rCCL18-induced OSCC. Furthermore, JAK2/STAT3 signalling was confirmed to be a downstream pathway of the CCL18-NIR1/GPR3 axis.Conclusion CCL18 can promote the progression of OSCC by binding specific receptors (NIR1 and GPR3), and the CCL18-receptor signalling can activate JAK2/STAT3 pathway. The identification of the mechanisms of CCL18 promoting OSCC progression could implicate potential therapeutic targets for treating oral cancer.

show abstract

Basic Transcription Factor 3 Is Required for Proliferation and Epithelial‐Mesenchymal Transition via Regulation of FOXM1 and JAK2/STAT3 Signaling in Gastric Cancer

Cited by 22 publications

References 23 publications

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

Bayesian differential analysis of gene regulatory networks exploiting genetic perturbations

CCL18-NIR1/GPR3 promotes oral cancer cell growth and metastasis by activating the JAK2/STAT3 signalling pathway

Contact Info

Product

Resources

About