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Wnt signal transduction pathway and apoptosis: a review.

ABSTRACT: The association between the wnt signaling pathway and apoptosis has become more firmly established in the recent scientific literature. Many reports indicate that the wnt signaling pathway regulates apoptosis through a variety of mechanisms.The activity of wnt signaling according to specific cellular environment stimuli can either foster or restrain the processes of apoptosis. Wnt signaling regulates the early and late stages of apoptosis in both development and cellular injury in populations of neurons, endothelial cells, vascular smooth muscle cells and cardiomyocytes.In this review I draw attention to genes and proteins of the wnt signaling pathway involved in apoptosis and describe some of their functional effects.

SUBMITTER: Pecina-Slaus N

PROVIDER: S-EPMC2908610 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature

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Wnt signal transduction pathway and apoptosis: a review.

Pećina-Slaus Nives N

Cancer cell international 20100630

The association between the wnt signaling pathway and apoptosis has become more firmly established in the recent scientific literature. Many reports indicate that the wnt signaling pathway regulates apoptosis through a variety of mechanisms.The activity of wnt signaling according to specific cellular environment stimuli can either foster or restrain the processes of apoptosis. Wnt signaling regulates the early and late stages of apoptosis in both development and cellular injury in populations of ...[more]

PMID: 20591184

Similar Datasets

Wnt signal transduction pathways: modules, development and evolution.

Project description:BackgroundWnt signal transduction pathway (Wnt STP) is a crucial intracellular pathway mainly due to its participation in important biological processes, functions, and diseases, i.e., embryonic development, stem-cell management, and human cancers among others. This is why Wnt STP is one of the highest researched signal transduction pathways. Study and analysis of its origin, expansion and gradual development to the present state as found in humans is one aspect of Wnt research. The pattern of development and evolution of the Wnt STP among various species is not clear till date. A phylogenetic tree created from Wnt STPs of multiple species may address this issue.ResultsIn this respect, we construct a phylogenetic tree from modules of Wnt STPs of diverse species. We term it as the 'Module Tree'. A module is nothing but a self-sufficient minimally-dependent subset of the original Wnt STP. Authenticity of the module tree is tested by comparing it with the two reference trees.ConclusionsThe module tree performs better than an alternative phylogenetic tree constructed from pathway topology of Wnt STPs. Moreover, an evolutionary emergence pattern of the Wnt gene family is created and the module tree is tallied with it to showcase the significant resemblances.

| S-EPMC4977476 | biostudies-literature

Signal transduction by the Wnt family of ligands.

Project description:The Wnt genes encode a large family of secreted polypeptides that mediate cell-cell communication in diverse developmental processes. The loss or inappropriate activation of Wnt expression has been shown to alter cell fate, morphogenesis and mitogenesis. Recent progress has identified Wnt receptors and components of an intracellular signalling pathway that mediate Wnt-dependent transcription. This review will highlight this 'core' Wnt signal-transduction pathway, but also aims to reveal the potential diversity of Wnt signalling targets. Particular attention will be paid to the overlap between developmental biology and oncogenesis, since recent progress shows Wnt signalling forms a paradigm for an interdisciplinary approach.

| S-EPMC1219034 | biostudies-other

Pancreatic cancer-derived exosomes induce apoptosis of T lymphocytes through the p38 MAPK signal transduction pathway

Project description:Pancreatic cancer is the fourth most lethal malignancy, which is characterized by poor immunogenicity. Pancreatic cancer cells take various strategies to suppress host immune response, evade immune defenses, and facilitate tumor growth and development. As a mode of long-range intercellular communication, cancer-derived exosomes contribute to the impairment of the immune system. However, the mechanisms that induce changes in the activities of signal transduction pathways in immune cells, which are influenced by tumor-derived exosomes, are poorly understood. We treated peripheral T lymphocytes with pancreatic cancer-derived exosomes, performed RNA-seq and Gene Set Enrichment Analysis to explore the pivotal signaling pathway that mediates apoptosis in exosomes-treated T lymphocytes.

2018-06-18 | GSE115831 | GEO

Signal transduction pathway of TonB-dependent transporters.

Project description:Transcription of the ferric citrate import system is regulated by ferric citrate binding to the outer membrane transporter FecA. A signal indicating transporter occupancy is relayed across the outer membrane to energy-transducing and regulatory proteins embedded in the cytoplasmic membrane. Because transcriptional activation is not coupled to ferric citrate import, an allosteric mechanism underlies this complex signaling mechanism. Using evolution-based statistical analysis we have identified a sparse but structurally connected network of residues that links distant functional sites in FecA. Functional analyses of these positions confirm their involvement in the mechanism that regulates transcriptional activation in response to ferric citrate binding at the cell surface. This mechanism appears to be conserved and provides the structural basis for the allosteric signaling of TonB-dependent transporters.

| S-EPMC1760641 | biostudies-literature

Substance P activates the Wnt signal transduction pathway and enhances the differentiation of mouse preosteoblastic MC3T3-E1 cells.

Project description:Recent experiments have explored the impact of Wnt/β-catenin signaling and Substance P (SP) on the regulation of osteogenesis. However, the molecular regulatory mechanisms of SP on the formation of osteoblasts is still unknown. In this study, we investigated the impact of SP on the differentiation of MC3T3-E1 cells. The osteogenic effect of SP was observed at different SP concentrations (ranging from 10⁻¹⁰ to 10⁻⁸ M). To unravel the underlying mechanism, the MC3T3-E1 cells were treated with SP after the pretreatment by neurokinin-1 (NK1) antagonists and Dickkopf-1 (DKK1) and gene expression levels of Wnt/β-catenin signaling pathway components, as well as osteoblast differentiation markers (collagen type I, alkaline phosphatase, osteocalcin, and Runx2), were measured using quantitative polymerase chain reaction (PCR). Furthermore, protein levels of Wnt/β-catenin signaling pathway were detected using Western blotting and the effects of SP, NK1 antagonist, and DKK1 on β-catenin activation were investigated by immunofluorescence staining. Our data indicated that SP (10⁻⁹ to 10⁻⁸ M) significantly up-regulated the expressions of osteoblastic genes. SP (10⁻⁸ M) also elevated the mRNA level of c-myc, cyclin D1, and lymphocyte enhancer factor-1 (Lef1), as well as c-myc and β-catenin protein levels, but decreased the expression of Tcf7 mRNA. Moreover, SP (10-8 M) promoted the transfer of β-catenin into nucleus. The effects of SP treatment were inhibited by the NK1 antagonist and DKK1. These findings suggest that SP may enhance differentiation of MC3T3-E1 cells via regulation of the Wnt/β-catenin signaling pathway.

| S-EPMC4013624 | biostudies-literature

?-catenin-mediated Wnt signal transduction proceeds through an endocytosis-independent mechanism.

Project description:The Wnt pathway is a key intercellular signaling cascade that regulates development, tissue homeostasis, and regeneration. However, gaps remain in our understanding of the molecular events that take place between ligand-receptor binding and target gene transcription. We used a novel tool for quantitative, real-time assessment of endogenous pathway activation, measured in single cells, to answer an unresolved question in the field-whether receptor endocytosis is required for Wnt signal transduction. We combined knockdown or knockout of essential components of clathrin-mediated endocytosis with quantitative assessment of Wnt signal transduction in mouse embryonic stem cells (mESCs). Disruption of clathrin-mediated endocytosis did not affect accumulation and nuclear translocation of ?-catenin, as measured by single-cell live imaging of endogenous ?-catenin, and subsequent target gene transcription. Disruption of another receptor endocytosis pathway, caveolin-mediated endocytosis, did not affect Wnt pathway activation in mESCs. Additional results in multiple cell lines support that endocytosis is not a requirement for Wnt signal transduction. We show that off-target effects of a drug used to inhibit endocytosis may be one source of the discrepancy among reports on the role of endocytosis in Wnt signaling.

| S-EPMC7353137 | biostudies-literature

Limited dishevelled/Axin oligomerization determines efficiency of Wnt/?-catenin signal transduction.

Project description:In Wnt/?-catenin signaling, the transcriptional coactivator ?-catenin is regulated by its phosphorylation in a complex that includes the scaffold protein Axin and associated kinases. Wnt binding to its coreceptors activates the cytosolic effector Dishevelled (Dvl), leading to the recruitment of Axin and the inhibition of ?-catenin phosphorylation. This process requires interaction of homologous DIX domains present in Dvl and Axin, but is mechanistically undefined. We show that Dvl DIX forms antiparallel, double-stranded oligomers in vitro, and that Dvl in cells forms oligomers typically <10 molecules at endogenous expression levels. Axin DIX (DAX) forms small single-stranded oligomers, but its self-association is stronger than that of DIX. DAX caps the ends of DIX oligomers, such that a DIX oligomer has at most four DAX binding sites. The relative affinities and stoichiometry of the DIX-DAX interaction provide a mechanism for efficient inhibition of ?-catenin phosphorylation upon Axin recruitment to the Wnt receptor complex.

| S-EPMC7200158 | biostudies-literature

Signal transduction pathway mutations in gastrointestinal (GI) cancers: a systematic review and meta-analysis.

Project description:The present study was conducted to evaluate the prevalence of the signaling pathways mutation rate in the Gastrointestinal (GI) tract cancers in a systematic review and meta-analysis study. The study was performed based on the PRISMA criteria. Random models by confidence interval (CI: 95%) were used to calculate the pooled estimate of prevalence via Metaprop command. The pooled prevalence indices of signal transduction pathway mutations in gastric cancer, liver cancer, colorectal cancer, and pancreatic cancer were 5% (95% CI: 3-8%), 12% (95% CI: 8-18%), 17% (95% CI: 14-20%), and 20% (95% CI: 5-41%), respectively. Also, the mutation rates for Wnt pathway and MAPK pathway were calculated to be 23% (95% CI, 14-33%) and 20% (95% CI, 17-24%), respectively. Moreover, the most popular genes were APC (in Wnt pathway), KRAS (in MAPK pathway) and PIK3CA (in PI3K pathway) in the colorectal cancer, pancreatic cancer, and gastric cancer while they were beta-catenin and CTNNB1 in liver cancer. The most altered pathway was Wnt pathway followed by the MAPK pathway. In addition, pancreatic cancer was found to be higher under the pressure of mutation compared with others based on pooled prevalence analysis. Finally, APC mutations in colorectal cancer, KRAS in gastric cancer, and pancreatic cancer were mostly associated gene alterations.

| S-EPMC7599243 | biostudies-literature

Signal transduction pathway profiling of individual tumor samples.

Project description:BackgroundSignal transduction pathways convey information from the outside of the cell to transcription factors, which in turn regulate gene expression. Our objective is to analyze tumor gene expression data from microarrays in the context of such pathways.ResultsWe use pathways compiled from the TRANSPATH/TRANSFAC databases and the literature, and three publicly available cancer microarray data sets. Variation in pathway activity, across the samples, is gauged by the degree of correlation between downstream targets of a pathway. Two correlation scores are applied; one considers all pairs of downstream targets, and the other considers only pairs without common transcription factors. Several pathways are found to be differentially active in the data sets using these scores. Moreover, we devise a score for pathway activity in individual samples, based on the average expression value of the downstream targets. Statistical significance is assigned to the scores using permutation of genes as null model. Hence, for individual samples, the status of a pathway is given as a sign, + or -, and a p-value. This approach defines a projection of high-dimensional gene expression data onto low-dimensional pathway activity scores. For each dataset and many pathways we find a much larger number of significant samples than expected by chance. Finally, we find that several sample-wise pathway activities are significantly associated with clinical classifications of the samples.ConclusionThis study shows that it is feasible to infer signal transduction pathway activity, in individual samples, from gene expression data. Furthermore, these pathway activities are biologically relevant in the three cancer data sets.

| S-EPMC1184060 | biostudies-literature

IMPACT: Unraveling intracellular signal transduction and pathway crosstalk by exploring pathway landscape

Project description:Understanding complicated modularization and crosstalk of intracellular signal transduction pathways holds the key to battle against drug resistance in human cancer research. We propose an integrative approach, namely Inferring Modularization of PAthway CrossTalk (IMPACT), to identify aberrant pathway modules and their between-module crosstalk by exploring pathway landscape that is reconstructed from a sampling strategy. The pathway identification method (i.e., IMPACT) was applied to breast cancer data to uncover aberrant pathway modules, which were further investigated with cell line studies to understand drug resistance in breast cancer. The patient datasets we mentioned are published and are available in the GEO database as GSE6532 and GSE17705. The re-processed GSE6532 and GSE17705 patient datasets are linked below as supplementary files. The GSE6532_matrix.txt and GSE17705_matrix.txt are processed by Affy Gene console with plier as normailization. But importantly, we also used 'Combat' method (http://www.bu.edu/jlab/wp-assets/ComBat/Abstract.html) to remove potential institutional batch effect. Four MCF7 derived cell models were included in the study: MCF7-STR, MCF7RR-STR, LCC1 and LCC2 cell lines. MCF7-STR and MCF7RR-STR were grown in phenol red-free IMEM supplemented with 5% charcoal-stripped calf serum and 1nM estradiol for 72 h prior to RNA extraction. LCC1 and LCC2 cells were grown in phenol red-free IMEM supplemented with 5% charcoal-stripped calf serum. The cell line data were used to validate computational results derived from patient datasets.

2013-09-07 | E-GEOD-50564 | biostudies-arrayexpress

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