&lt;p&gt;New Advances in Canonical Wnt/β-Catenin Signaling in Cancer&lt;/p&gt;

Wen, Xiaolan; Wu, Yanling; Awadasseid, Annoor; Tanaka, Yoshimasa; Zhang, Wen

doi:10.2147/cmar.s258645

Cited by 52 publications

(37 citation statements)

References 78 publications

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“…The Wnt gene was first identified in mice, called Int-1. It is named Wnt because of its high homology with the wingless gene of Drosophila melanogaster 5 , 6 . The Wnt pathway plays an important role in regulating embryonic development and cell differentiation 5 , 6 .…”

Section: Introductionmentioning

confidence: 99%

“…It is named Wnt because of its high homology with the wingless gene of Drosophila melanogaster 5 , 6 . The Wnt pathway plays an important role in regulating embryonic development and cell differentiation 5 , 6 . Abnormalities in Wnt/β-catenin signaling have been found in many tumors, including NSCLC, and play important roles in cancer progression 7 .…”

Section: Introductionmentioning

confidence: 99%

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ATF4 promotes lung cancer cell proliferation and invasion partially through regulating Wnt/β-catenin signaling

Du¹,

Liu²,

Mao³

et al. 2021

Int. J. Med. Sci.

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Activating transcription factor 4 (ATF4) is a member of the cAMP response element binding (CREB) protein family and has been reported to participate in cancer progression; however, its molecular mechanism is not fully understood. In this study, we investigated the function of ATF4 in non-small cell lung cancer and its molecular regulation. We detected cytoplasmic and nuclear ATF4 expression in lung cancer A549, H1299, and LK2 cells, and the total expression of ATF4 was higher than that in HBE cells ( p < 0.05). Higher nuclear ATF4 expression was detected in all these cells compared to cytoplasmic ATF4 expression ( p < 0.05). Overexpression of ATF4 in A549 cells significantly promoted cancer cell growth and invasion ( p < 0.05). Expression of Wnt signaling molecules, including β-catenin, MMP7, and cyclin D1, and the activity of canonical Wnt signaling were also significantly promoted by ATF4 ( p < 0.05). ICG001, a canonical Wnt signaling inhibitor that selectively inhibits β-catenin/ cyclic adenosine monophosphate response element binding protein (CBP) interaction, significantly inhibited cancer cell invasion and Wnt signaling. The function of ATF4 was also significantly inhibited by ICG001 ( p < 0.05). However, compared to treatment with ICG001, the invasion ability of cancer cells treated with both ICG001 and ATF4 cDNA significantly increased ( p < 0.05), which indicates that the function of ATF4 was not dependent only on Wnt/β-catenin signaling. The function of ATF4 in the regulation of β-catenin expression was not significantly affected by ICG001 ( p > 0.05). The function of ATF4 to promote the activity of Wnt/β-catenin signaling in cancer cells was abolished by treatment with ICG001 ( p > 0.05). These results indicate that ATF4 may contribute to lung cancer progression at least partly by regulating Wnt/β-catenin signaling.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ATF4 promotes lung cancer cell proliferation and invasion partially through regulating Wnt/β-catenin signaling

Du¹,

Liu²,

Mao³

et al. 2021

Int. J. Med. Sci.

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show abstract

“…The Wnt/β-catenin signaling pathway has been reported to be related to the oncogenesis and progression of multiple kinds of human cancers [ 15 – 17 ]. β-catenin is considered a positive regulator of this pathway that functions by promoting the transcription of target genes [ 29 ]. Some target genes, such as MMP9 and cyclin D1, are involved in oncogenesis, regulating cancer proliferation and metastasis [ 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

Oncogenic UBE3C promotes breast cancer progression by activating Wnt/β-catenin signaling

et al. 2021

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Background Breast cancer (BrCa) is the most common female malignancy worldwide and has the highest morbidity among all cancers in females. Unfortunately, the mechanisms of BrCa growth and metastasis, which lead to a poor prognosis in BrCa patients, have not been well characterized. Methods Immunohistochemistry (IHC) was performed on a BrCa tissue microarray (TMA) containing 80 samples to evaluate ubiquitin protein ligase E3C (UBE3C) expression. In addition, a series of cellular experiments were conducted to reveal the role of UBE3C in BrCa. Results In this research, we identified UBE3C as an oncogenic factor in BrCa growth and metastasis for the first time. UBE3C expression was upregulated in BrCa tissues compared with adjacent breast tissues. BrCa patients with high nuclear UBE3C expression in tumors showed remarkably worse overall survival (OS) than those with low nuclear expression. Knockdown of UBE3C expression in MCF-7 and MDA-MB-453 BrCa cells inhibited cell proliferation, migration and invasion in vitro, while overexpression of UBE3C in these cells exerted the opposite effects. Moreover, UBE3C promoted β-catenin nuclear accumulation, leading to the activation of the Wnt/β-catenin signaling pathway in BrCa cells. Conclusion Collectively, these results imply that UBE3C plays crucial roles in BrCa development and progression and that UBE3C may be a novel target for the prevention and treatment of BrCa.

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“…Yoko Katsuno et al research shows that TGF-β signaling and epithelial-mesenchymal transition in cancer progression. Furthermore, Wen et al 39 research indicated that the ectopic activation of Wnt/β-catenin-mediated signaling pathway can lead to a variety of tumors and diseases. This pathway not only plays an important role in proliferation, differentiation, apoptosis, migration, and invasion, but also plays an important role in the invasion and metastasis of cancer in epithelial-mesenchymal transition.…”

Section: Discussionmentioning

confidence: 99%

Construction and Validation of a Prognostic Model of Gastric Cancer with 10RBPs Based on 6 Microarrays

Zhou

Hao

Lin

et al. 2020

Preprint

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For explore the potential connection of RNA binding proteins (RBPs) to the expression function of gastric cancer (GC). We download the GPL10558 and GPL6947 platform mircroarray data from Gene Expression Omnibus (GEO) and Express database. Then the system integrates and analyzes the differentially expressed RBPs. And enrich the differentially expressed RBPs to understand the mechanism of its influence on tumors. Univariate Cox, lasso regression and multivariate Cox regression analysis were used to screen independent prognostic parameters to construct prognostic model, and calculate aera under time-dependent receiver operating characteristics (AUC) and survival analysis were used to evaluate their prognostic ability. GSE15459, GSE62254 cohorts were used to verify hub signature. Finally, we also verified the prognosis and expression of hub-RBPs. Systematic analysis identified 23 up-regulated and 30 down-regulated RBPs, and enrichment analysis showed that they mainly affect their modification by binding to mRNA, and their stability affects the progression of GC. After multiple statistical analyses, we obtained the prognostic signature constructed by 10 RBPs and determined that it has better predictive performance (AUC = 0.685). Through comprehensive bioinformatics analysis, we have obtained 10 key gastric cancer RBPs as potential prognostic biomarkers, providing new perspectives for the treatment and prognostic of GC.

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<p>New Advances in Canonical Wnt/β-Catenin Signaling in Cancer</p>

Cited by 52 publications

References 78 publications

ATF4 promotes lung cancer cell proliferation and invasion partially through regulating Wnt/β-catenin signaling

ATF4 promotes lung cancer cell proliferation and invasion partially through regulating Wnt/β-catenin signaling

Oncogenic UBE3C promotes breast cancer progression by activating Wnt/β-catenin signaling

Construction and Validation of a Prognostic Model of Gastric Cancer with 10RBPs Based on 6 Microarrays

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