Diverse LEF/TCF Expression in Human Colorectal Cancer Correlates with Altered Wnt-Regulated Transcriptome in a Meta-Analysis of Patient Biopsies

Mayer, Claus; Giclais, Soizick Magon de La; Alsehly, Fozan; Hoppler, Stefan

doi:10.3390/genes11050538

Cited by 13 publications

(13 citation statements)

References 62 publications

(92 reference statements)

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“…TCF7L2 plays a significant role in the pathogenesis of human cancers. A recent study ( 13 ) demonstrated that LEF/TCF-specific transcriptional regulation of Wnt target genes is associated with cancer progression and survival in human colorectal tumor samples.…”

Section: Introductionmentioning

confidence: 99%

Expression of TCF7L2 in Glioma and Its Relationship With Clinicopathological Characteristics and Patient Overall Survival

et al. 2021

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Background: The TCF7L2 gene is known as transcription factor 7-like 2 which has been identified as a novel transcription factor epithelial-mesenchymal transition (EMT) in tumor cells at 10q25.3. TCF7L2 may affect cancer progression and plays a central role in cancer proliferation, migration, and invasion. However, its clinical and prognostic value have not been researched in glioma. The purpose of our study was to research TCF7L2 expression and evaluate the clinical value of prognosis.Method: We collected glioma specimens including low-grade glioma (n = 46) and glioblastoma (n = 51) from September 2015 to September 2017. Expression of TCF7L2 in 97 specimens was detected by quantitative real-time PCR (qRT-PCR). The chi-square test was applied to analyze the relationship between TCF7L2 expression and clinicopathological characteristics. The overall survival (OS) was estimated by log-rank tests among strata, and the survival curves were drawn by Kaplan-Meier. Univariate and multivariate analysis were utilized to analyze the relationship between prognosis and clinicopathological characteristics including TCF7L2 expression.Results: Compared with the low-grade glioma group, the expression of TCF7L2 was significantly increased in the glioblastoma group (p = 0.001). TCF7L2 overexpression was associated with higher WHO grade (p = 0.001), isocitrate dehydrogenase (IDH) wild-type (p = 0.001), and lack of O(6)-methylguanine-DNA methyltransferase (MGMT) methylation (p = 0.001). Moreover, Kaplan-Meier analysis proved that overexpressed TCF7L2 was associated with poor OS (p = 0.010). The multivariate analysis suggested that TCF7L2 expression was an independent prognostic factor (p = 0.020).Conclusions: Our research proved that TCF7L2 was overexpressed in glioblastoma, and related with tumor long-term prognosis, which, therefore, could be an independent prognostic factor for glioma patients.

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Section: Introductionmentioning

confidence: 99%

Expression of TCF7L2 in Glioma and Its Relationship With Clinicopathological Characteristics and Patient Overall Survival

et al. 2021

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“…Nonoverlapping TCF/LEF functions have also been recently suggested in a meta‐analysis of gene expression data from human CRC transcriptomics datasets. The expression of individual TCF7 , LEF1 , TCF7L1 , and TCFL2 genes correlated with transcriptomes that are both quantitatively and qualitatively different, supporting branching transcriptional regulation of Wnt target genes by different TCF/LEF during CRC progression (Mayer, de La Giclais, Alsehly, & Hoppler, 2020 ). Many might be the additional functions that TCF/LEF sustain, but their central role in the transduction of the Wnt/β‐catenin pathway holds true even when challenged with the scrutiny of state‐of‐the‐art high‐throughput approaches—with only a few exceptions (see Section 3.3 ).…”

Section: β‐Catenin Sits On Dna: Tcf/lef Dependent and Independent Reg...mentioning

confidence: 73%

The WNT/β‐catenin dependent transcription: A tissue‐specific business

Söderholm

Cantù

2020

WIREs Mechanisms of Disease

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β‐catenin‐mediated Wnt signaling is an ancient cell‐communication pathway in which β‐catenin drives the expression of certain genes as a consequence of the trigger given by extracellular WNT molecules. The events occurring from signal to transcription are evolutionarily conserved, and their final output orchestrates countless processes during embryonic development and tissue homeostasis. Importantly, a dysfunctional Wnt/β‐catenin pathway causes developmental malformations, and its aberrant activation is the root of several types of cancer. A rich literature describes the multitude of nuclear players that cooperate with β‐catenin to generate a transcriptional program. However, a unified theory of how β‐catenin drives target gene expression is still missing. We will discuss two types of β‐catenin interactors: transcription factors that allow β‐catenin to localize at target regions on the DNA, and transcriptional co‐factors that ultimately activate gene expression. In contrast to the presumed universality of β‐catenin's action, the ensemble of available evidence suggests a view in which β‐catenin drives a complex system of responses in different cells and tissues. A malleable armamentarium of players might interact with β‐catenin in order to activate the right “canonical” targets in each tissue, developmental stage, or disease context. Discovering the mechanism by which each tissue‐specific β‐catenin response is executed will be crucial to comprehend how a seemingly universal pathway fosters a wide spectrum of processes during development and homeostasis. Perhaps more importantly, this could ultimately inform us about which are the tumor‐specific components that need to be targeted to dampen the activity of oncogenic β‐catenin. This article is categorized under: Cancer > Molecular and Cellular Physiology Cancer > Genetics/Genomics/Epigenetics Cancer > Stem Cells and Development

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“…(5) Secretory glycoprotein regulates the activation through butyrate acid. Accumulated β-Catenin in the cytoplasm enters the nucleus and binds the TCF transcription factor family to initiate the transcription of downstream target genes and inhibit cancer cells [80].…”

Section: Intestinal Flora and Its Metabolites Can Modulate Risk Of Tu...mentioning

confidence: 99%

The Role of Intestinal Flora in Anti-Tumor Antibiotic Therapy

Ye¹,

Wang²,

Lin³

et al. 2022

Front. Biosci. (Landmark Ed)

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Anti-tumor antibiotics are chemical substances produced by micro-organisms to control cancer development. Some of the currently used cancer treatment regimens are anti-tumor antibiotics. However, many studies have demonstrated that anti-tumor antibiotics may have adverse effects on normal cells. This calls for development of strategies to alleviate these negative effects and improve cancer treatment. Recent studies have suggested that the efficacy of anti-tumor antibiotics may be affected by intestinal microbiota. For instance, intestinal microbiota can alleviate the negative effects of antibiotic treatment and regulate the tumor immune micro-environment. In this way, anti-tumor antibiotics can improve tumor control. However, the specific mechanisms need to be further explored. This review discusses the effect of intestinal flora on anti-tumor antibiotic therapy and summarizes the specific mechanisms by which antibiotics inhibit harmful intestinal micro-organisms and promote efficacy of probiotics, which may improve the control of neoplasm development and growth.

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Diverse LEF/TCF Expression in Human Colorectal Cancer Correlates with Altered Wnt-Regulated Transcriptome in a Meta-Analysis of Patient Biopsies

Cited by 13 publications

References 62 publications

Expression of TCF7L2 in Glioma and Its Relationship With Clinicopathological Characteristics and Patient Overall Survival

Expression of TCF7L2 in Glioma and Its Relationship With Clinicopathological Characteristics and Patient Overall Survival

The WNT/β‐catenin dependent transcription: A tissue‐specific business

The Role of Intestinal Flora in Anti-Tumor Antibiotic Therapy

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