Multiple oncogenic roles of nuclear β-catenin

Kumar, Ranjeet; Bashyam, Murali D.

doi:10.1007/s12038-017-9710-9

Cited by 18 publications

(18 citation statements)

References 185 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cellular β-catenin exists in three different pools: membranous, cytoplasmic, and nuclear [19]. Freshly synthesized β-catenin interacts with E-cadherin and serves as a structural protein localized to the cell membrane (membranous pool).…”

Section: Main Textmentioning

confidence: 99%

“…In contrast, destruction complex captures free β-catenin in the cytoplasm and rapidly targets it for degradation (cytoplasmic pool). Due to the compromised function of the destruction complex, β-catenin escapes degradation and translocates into the nucleus (nuclear pool) [19]. In different cell pools, β-catenin undergoes distinct regulation patterns and have diverse functions.…”

Section: Main Textmentioning

confidence: 99%

See 1 more Smart Citation

β-Catenin: oncogenic role and therapeutic target in cervical cancer

Wang

Liu

et al. 2020

Biol Res

View full text Add to dashboard Cite

Cervical cancer is a common and fatal malignancy of the female reproductive system. Human papillomavirus (HPV) is the primary causal agent for cervical cancer, but HPV infection alone is insufficient to cause the disease. Actually, most HPV infections are sub-clinical and cleared spontaneously by the host immune system; very few persist and eventually develop into cervical cancer. Therefore, other host or environmental alterations could also contribute to the malignant phenotype. One of the candidate co-factors is the β-catenin protein, a pivotal component of the Wnt/βcatenin signaling pathway. β-Catenin mainly implicates two major cellular activities: cell-cell adhesion and signal transduction. Recent studies have indicated that an imbalance in the structural and signaling properties of β-catenin leads to various cancers, such as cervical cancer. In this review, we will systematically summarize the role of β-catenin in cervical cancer and provide new insights into therapeutic strategies.

show abstract

Section: Main Textmentioning

confidence: 99%

Section: Main Textmentioning

confidence: 99%

β-Catenin: oncogenic role and therapeutic target in cervical cancer

Wang

Liu

et al. 2020

Biol Res

View full text Add to dashboard Cite

show abstract

“…β-Catenin-mediated signaling regulates tumor initiation and progression in multiple malignancies [26]. Here, we analyzed the transcriptome data of esophageal cancer via the UALCAN data portal and found that the majority of genes in the pathway were differentially expressed in tumor tissues compared to normal tissues (Fig.…”

Section: Apatinib Regulated β-Catenin Signaling In Esophageal Cancermentioning

confidence: 99%

Apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer via the Akt/β-catenin pathway

Wei

Wang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Esophageal cancer is the sixth leading cause of cancer-related mortality worldwide, which is partially due to limited progress of therapy. Apatinib, an inhibitor of VEGFR2, has a promising antitumor effect on malignancies. However, the underlying mechanism of its antitumor effect on esophageal cancer remains poorly understood. Materials and methods: Eighteen pairs of frozen esophageal cancer and their para-cancer samples and 25 paraffin specimens from advanced esophageal cancer patients treated with cisplatin-based regimen were collected. The effects of apatinib on cell growth, cell apoptosis, cell cycle and invasion/migration of esophageal cancer cells were assessed. Bioinformatics, luciferase reporter, immunoprecipitation and immunofluorescence assays were conducted for mechanic investigation. Quantitative RT-PCR, western blotting and immunohistochemistry were used to measure the expression of functional genes. Xenograft tumor growth of mice was performed. Results: We found that VEGFR2 was highly expressed in esophageal cancer and associated with poor efficacy of cisplatin-based treatment. Apatinib displayed profound actions against tumor cell growth of human esophageal cancer via promoting cell apoptosis and cell cycle arrest. Also, apatinib displayed the inhibitory effects on cell migration and invasion. Moreover, apatinib strongly suppressed the growth of esophageal cancer xenografts in mice. The effects of apatinib on esophageal cancer were partially dependent on its block of the VEGFR2/Akt/β-catenin pathway. Specifically, apatinib induced the degradation of β-catenin and decreased its transcriptional activity through Akt/GSK-3β repression. Further in vitro and in vivo studies revealed that low dose apatinib had a synergistic antitumor effect with cisplatin on esophageal cancer. Conclusion: Our study indicates that apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer by deactivating the Akt/β-catenin pathway. These findings provide a theoretical foundation for using apatinib as an effective therapeutic drug for esophageal cancer.

show abstract

“…Nuclear positivity of β-catenin as a result of activated Wnt pathway has been previously detected in many other tumors (27). However, more recent studies show, that the translocation of β-catenin to nucleus is more likely a multi-factorial process than just a result of cytosolic accumulation of this molecule, even if the Wnt pathway is activated (28).…”

Section: Discussionmentioning

confidence: 94%

Expression of molecules of the Wnt pathway and of E‑cadherin in the etiopathogenesis of human thymomas

et al. 2020

View full text Add to dashboard Cite

The molecular pathogenesis of thymoma remains largely unknown. It has been recently demonstrated, that activation of Wnt signaling pathway leads to increased incidence of thymoma in murine models. The present study investigated the activation of molecules of the Wnt signaling pathway in human thymoma. A total of 112 thymoma cases with complete clinical and follow-up data and 8 controls were included in the present study. Patients with thymoma and controls were examined immunohistochemically for β-catenin and E-cadherin. The mRNA expression levels of CTNNB1, CCND1, MYC, A XIN2 and CDH1 were analyzed by reverse transcription-quantitative PCR. Immunohistochemically, β-catenin and E-cadherin were overexpressed in neoplastic cells of all thymomas. In type A, B1 and non-invasive type B2 thymoma, both molecules were located in the cytoplasm, in contrast to invasive type B2 and B3 thymoma, where membranous immunopositivities were observed. mRNA expression levels of genes involved in the Wnt pathway and of E-cadherin were significantly increased in both type A and B thymoma compared with controls; increasing gradually from type B1 to B3, and with higher stage of disease. In recurrent type B thymoma, the mRNA expression of the molecules was significantly higher. Despite the activation of Wnt pathway in indolent type A thymoma, the negative feedback of the pathway was preserved by overexpression of inhibitory molecule axin2, which was not overexpressed in type B thymoma. In summary, the Wnt pathway was activated in human thymoma and may contribute to oncogenesis. Detection of molecules of the Wnt pathway may be of diagnostic and prognostic value.

show abstract

Multiple oncogenic roles of nuclear β-catenin

Cited by 18 publications

References 185 publications

β-Catenin: oncogenic role and therapeutic target in cervical cancer

β-Catenin: oncogenic role and therapeutic target in cervical cancer

Apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer via the Akt/β-catenin pathway

Expression of molecules of the Wnt pathway and of E‑cadherin in the etiopathogenesis of human thymomas

Contact Info

Product

Resources

About