Wnt inhibitory factor-1 functions as a tumor suppressor through modulating Wnt/β-catenin signaling in neuroblastoma

Zhang, Jiao; Zhou, Bin; Liu, Yinghua; Chen, Keling; Bao, Pingqian; Wang, Yi; Wang, Jiaxiang; Zhou, Zong-Guang; Sun, Xiao‐Feng; Li, Yuan

doi:10.1016/j.canlet.2014.02.011

Cited by 35 publications

(27 citation statements)

References 45 publications

(60 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The general opposite control has been considered to be mediated by Wnt antagonists such as endogenic DKK-1, SFRP-1 and Wif-1. The main inhibitory mechanism is the interference of the combination between Wnt and its receptors (14,(30)(31)(32)(33). Fig.…”

Section: The Level Of Dkk-1 and Sfrp-1 Inversely Regulate The Inos Anmentioning

confidence: 99%

Effect of nitric oxide synthase on multiple drug resistance is related to Wnt signaling in non-small cell lung cancer

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

Multiple drug resistance (MDR) is considered a major challenge in the clinical treatment of non-small cell lung cancer (NSCLC). Both nitric oxide synthase (iNOS) and Wnt signaling pathway participate in the regulation of drug resistance, but the interaction between them remains unclear. In the present study, we detected the activation of Wnt/β-catenin signaling in iNOS-induced drug-resistant lung cancer cells, and compared the effect of canonical and noncanonical Wnt pathway on the level of iNOS. Moreover, we investigated the expression of Wnt/β-catenin signaling downstream factors and its main inhibitors. The results indicated iNOS-induced drug resistance was possibly mediated by glutathione S-transferase-π (GST-π) and topoisomerase IIα (TOPO IIα), but not P-glycoprotein (P-gp), and this process was closely associated with the activation of canonical Wnt/β-catenin signaling, but less with noncanonical pathways. The mechanism of iNOS promoting Wnt/β-catenin pathway was mainly dependent on the inverse regulation of Dickkopf-1 (DKK-1) and secreted frizzled-related protein-1 (SFRP-1). Clarifying the relationship between iNOS and Wnt signaling may provide insight into a better understanding of the mechanism of drug resistance development in NSCLC.

show abstract

Section: The Level Of Dkk-1 and Sfrp-1 Inversely Regulate The Inos Anmentioning

confidence: 99%

Effect of nitric oxide synthase on multiple drug resistance is related to Wnt signaling in non-small cell lung cancer

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…Histone modification and promoter CpG methylation alter cancer-related gene expression and are frequently involved in carcinogenesis [58] . So far, downregulation of Wnt antagonist genes associated to promoter hypermethylation have been identified in a variety of malignancies, such as renal, bladder, lung, breast, colorectal, gastric and neuroblastoma [59][60][61][62][63][64][65] . Furthermore, the Wnt/b-catenin pathway genes are found among those affected by dysregulation of microRNAs (miRNAs) in many kinds of cancers, and particularly, expression profiling has shown that certain miRNAs are associated with gastric cancer development, progression and response to therapy [66][67][68] .…”

mentioning

confidence: 99%

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Chiurillo

2015

WJEM

261

219

View full text Add to dashboard Cite

Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput "omics" approaches will help in the search for Wnt pathway antagonist in the near future.

show abstract

“…The WNT/β-catenin signaling pathway has been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis [31]. This pathway supports stem and cancer stem cells [32].…”

Section: Discussionmentioning

confidence: 99%

MCL-1 plays an oncogenic role in breast cancer by modulating chemoresistance and stemness properties by activating Wnt/β-catenin

Zhang

Zhu

Zhang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Breast cancer is the most common malignant tumor and the leading cause of death in women. Chemotherapy is one of the most important treatments for breast cancer. However, the development of chemotherapy resistance is the main cause of 20–30% of breast cancer patients developing metastasis, leading to death. MCL-1, an anti-apoptotic protein, has not been found to contribute to chemotherapy resistance in breast cancer. Methods We used large gene panels to detect pathological sections of tumors in drug-resistant and sensitive patients. We validated protein profiling by IHC in a larger cohort of samples. We performed the function of MCL-1 by knockdown and overexpression in vitro and in vivo. Luciferase assay and CHIP assay were used to prove the regulatory network between MCL-1 and LRP6. Result We found that MCL-1 is more highly expressed in drug-resistant breast cancer tissues than it is in sensitive breast cancer tissues. Functional studies have revealed that MCL-1 plays an important role in drug resistance by regulating apoptosis in breast cancer cells. We found that overexpression of MCL-1 enhances the chemoresistance and stemness of breast cancer cells in vitro and in vivo, while silencing has the opposite effect. Mechanistically, by downregulating and upregulating MCL-1, we show that MCL-1 regulates LRP6 and activates the WNT/β-catenin signaling pathway in breast cancer cells. Finally, we found that a high level of MCL-1 expression predicts a poor prognosis in breast cancer. Conclusion Our work highlights the role of MCL-1 in chemoresistance and stemness. The MCL-1-WNT/β-catenin axis might be used as a new clinical target for breast cancer therapy.

show abstract

Wnt inhibitory factor-1 functions as a tumor suppressor through modulating Wnt/β-catenin signaling in neuroblastoma

Cited by 35 publications

References 45 publications

Effect of nitric oxide synthase on multiple drug resistance is related to Wnt signaling in non-small cell lung cancer

Effect of nitric oxide synthase on multiple drug resistance is related to Wnt signaling in non-small cell lung cancer

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

MCL-1 plays an oncogenic role in breast cancer by modulating chemoresistance and stemness properties by activating Wnt/β-catenin

Contact Info

Product

Resources

About