The interaction of canonical Wnt/β-catenin signaling with protein lysine acetylation

You, Hua; Li, Qi; Kong, Delong; Liu, Xiangye; Kong, Fanyun; Zheng, Kuiyang; Tang, Renxian

doi:10.1186/s11658-021-00305-5

Cited by 28 publications

(19 citation statements)

References 99 publications

(105 reference statements)

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“…CSNK1D was discovered to potentially interact with DVLs via proteinprotein interaction (PPI) prediction. The DVLs interactome is a well-known regulator of the Wnt pathway, which facilitate inhibition of the destruction complex targeting β-catenin at the cell membrane [39,40]. According to the experimental validation, knockdown of CSNK1D could only inhibit the expression of DVL3 rather than DVL1 or DVL2.…”

Section: Discussionmentioning

confidence: 99%

Circadian gene CSNK1D promoted the progression of hepatocellular carcinoma by activating Wnt/β-catenin pathway via stabilizing Dishevelled Segment Polarity Protein 3

et al. 2022

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Purpose A variety of studies have connected circadian rhythm to the initiation and progression of hepatocellular carcinoma (HCC). The purpose of this study was to figure out about the circadian genes' profile characteristics, prognostic significance, and targeted values in HCC. Methods The expression profiles and prognostic significance of circadian genes in the cancer genome atlas liver hepatocellular carcinoma (TCGA-LIHC) database were investigated using bioinformatics analysis. The expression features of Casein Kinase 1 Delta (CSNK1D), a robust signature gene, was further detected by immunohistochemistry, western blotting and Real-time quantitative PCR (RT-qPCR) in a local HCC cohort. The effect of CSNK1D on corresponding phenotypes of HCC cells was evaluated using Cell Counting Kit-8 (CCK8), flowcytometry, clone assay, Transwell assay, and xenograft assay. In addition, the underlying mechanisms of CSNK1D in the Wnt/β-catenin signaling were validated by multiple molecular experiments. Results Abnormal expression of the Circadian genome was associated with the malignant clinicopathological characteristics of HCC patients. A 10 circadian gene-based signature with substantial prognostic significance was developed using Cox regression and least absolute shrinkage and selection operator (LASSO) analysis. Of them, CSNK1D, significantly elevated in a local HCC cohort, was chosen for further investigation. Silencing or overexpression of CSNK1D significantly reduced or increased proliferation, invasion, sorafenib resistance, xenograft development, and epithelial-mesenchymal transformation (EMT) of HCC cells, respectively. Mechanically, CSNK1D exacerbated the aggressiveness of HCC cells by activating Wnt/β-catenin signaling through interacting with Dishevelled Segment Polarity Protein 3 (DVL3). Conclusions The Circadian gene CSNK1D was found to contribute to HCC progression by boosting the Wnt/β-catenin pathway, hinting that it could be a prospective therapeutic target for HCC.

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Section: Discussionmentioning

confidence: 99%

Circadian gene CSNK1D promoted the progression of hepatocellular carcinoma by activating Wnt/β-catenin pathway via stabilizing Dishevelled Segment Polarity Protein 3

et al. 2022

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“…The relationship between lysine acetylation and Wnt/β-catenin signaling pathway is of great significance to the occurrence and progression of tumors. Histone lysine acetylation can regulate the transcription of important biomolecules in the Wnt/β-catenin signaling pathway, while non-histones Lysine acetylation directly alters the function of core molecules in Wnt/β-catenin signaling pathway [36]. Previous studies have shown that the Wnt/β-catenin signaling pathway plays an important role in the occurrence and progression of osteosarcoma [37,39].…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0087302, a circular RNA, affects the progression of osteosarcoma via the Wnt/β-catenin signaling pathway

Peng¹,

Liu²,

Wu³

et al. 2022

Int. J. Med. Sci.

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Osteosarcoma is the most common malignant tumor in adolescent bone malignancies. It has the characteristics of a high metastasis rate, high mortality and poor prognosis. As a subclass of endogenous noncoding RNAs, circRNAs have been identified to be related to the occurrence, development and prognosis of different kinds of cancers, but the mechanism of their effect on osteosarcoma is not clear. In the present study, we identified a novel circRNA, hsa_circ_0087302, by RNA-seq, and we found that it was expressed at low levels in osteosarcoma. Using RT-PCR, we confirmed that the expression of hsa_circ_0087302 in osteosarcoma cells was lower than that in osteoblasts. Functional validation experiments revealed that hsa_circ_0087302 overexpression inhibited proliferation, cell cycle, migration, and invasion in osteosarcoma cells. Furthermore, Western blotting experiments demonstrated that hsa_circ_0087302 affected the expression of cell cycle-and Wnt/β-catenin signaling pathway-related proteins. For the first time, we identified that hsa_circ_0087302 may affect the malignant biological behavior of osteosarcoma cells through the Wnt/β-catenin signaling pathway. In summary, hsa_circ_0087302 may provide a new direction for the diagnosis and treatment of osteosarcoma.

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“…Interaction of Wnt and receptor leads to Axin and Disheveled proteins being recruited to the cell membrane and inhibits glycogen synthase kinase (GSK)-3β protein. β-Catenin can trigger GSK-3β to negatively regulate the Wnt pathway [ 34 – 36 , 42 , 43 ]. Notably, GSK-3β inhibition causes accumulation of β-catenin in the cytoplasm and paves the way for its translocation into the nucleus.…”

Section: Major Signaling Pathways In Breast Cancermentioning

confidence: 99%

The role of epigenetic modifications in drug resistance and treatment of breast cancer

et al. 2022

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Background Breast cancer is defined as a biological and molecular heterogeneous disorder that originates from breast cells. Genetic predisposition is the most important factor giving rise to this malignancy. The most notable mutations in breast cancer occur in the BRCA1 and BRCA2 genes. Owing to disease heterogeneity, lack of therapeutic target, anti-cancer drug resistance, residual disease, and recurrence, researchers are faced with challenges in developing strategies to treat patients with breast cancer. Results It has recently been reported that epigenetic processes such as DNA methylation and histone modification, as well as microRNAs (miRNAs), have potently contributed to the pathophysiology, diagnosis, and treatment of breast cancer. These observations have persuaded researchers to move their therapeutic approaches beyond the genetic framework toward the epigenetic concept. Conclusion Herein we discuss the molecular and epigenetic mechanisms underlying breast cancer progression and resistance as well as various aspects of epigenetic-based therapies as monotherapy and combined with immunotherapy.

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The interaction of canonical Wnt/β-catenin signaling with protein lysine acetylation

Cited by 28 publications

References 99 publications

Circadian gene CSNK1D promoted the progression of hepatocellular carcinoma by activating Wnt/β-catenin pathway via stabilizing Dishevelled Segment Polarity Protein 3

Circadian gene CSNK1D promoted the progression of hepatocellular carcinoma by activating Wnt/β-catenin pathway via stabilizing Dishevelled Segment Polarity Protein 3

Hsa_circ_0087302, a circular RNA, affects the progression of osteosarcoma via the Wnt/β-catenin signaling pathway

The role of epigenetic modifications in drug resistance and treatment of breast cancer

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