Wnt/β-catenin-driven EMT regulation in human cancers

Xue, Wenhua; Yang, Lin; Chen, Chengxin; Ashrafizadeh, Milad; Tian, Yu; Sun, Ranran

doi:10.1007/s00018-023-05099-7

Cited by 22 publications

(5 citation statements)

References 225 publications

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“…Finally, a connecting link between the UPS and adhesion is also the transcription regulator β-catenin, a molecule that has also been correlated with cancer invasiveness and EMT (52). The resistant clones exhibited increased β-catenin accumulation, an observation in accordance with the protein’s role as an oncogene (53).…”

Section: Resultsmentioning

confidence: 99%

The ERK1/2-Elk1, JNK-cJun, and JAK-STAT Transcriptional Axes as Potential Bortezomib Resistance Mediators in Prostate Cancer

Kalampounias,

Zafeiropoulou,

Androutsopoulou

et al. 2024

Preprint

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The effectiveness of proteasome inhibitors against solid tumors is limited as the emergence of resistance is rapid. Although many mechanisms have been proposed and verified, no definite answer has been given, highlighting the complexity of the resistant phenotype. In this study, a Bortezomib-resistant prostate cancer cell line is created, and a broad-spectrum signaling pathway analysis is performed to identify differences and adaptations the resistant cells exhibit. Our findings highlight the upregulation and activation of Nf-κB, STAT3, cJun, and Elk1 transcription factors in the resistant cells and the subsequent evasion of apoptosis and induction of autophagy, which is constantly activated and substitutes the role of the ubiquitin-proteasome system (UPS). Additionally, assessment of the intracellular reactive oxygen species in resistant cells confirms their downregulation, which is theorized to be a consequence of metabolic changes, increased autophagic flux, and antioxidative enzyme action. The results of this study highlight the potential therapeutic targeting of key kinases and transcription factors, participating in the main signaling pathways and gene regulation of Bortezomib-resistant cells, that could re-sensitize the cells to proteasome inhibitors, thus surpassing the current limitations.

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Section: Resultsmentioning

confidence: 99%

The ERK1/2-Elk1, JNK-cJun, and JAK-STAT Transcriptional Axes as Potential Bortezomib Resistance Mediators in Prostate Cancer

Kalampounias,

Zafeiropoulou,

Androutsopoulou

et al. 2024

Preprint

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show abstract

“…It regulates various biological processes by controlling gene expression and cell fate. In certain circumstances, the abnormal activation of the Wnt/β-Catenin signaling pathway can promote the development of cancer [ 50 – 52 ]. This often involves the excessive accumulation of β-Catenin protein and its increased activity within the cell nucleus.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of SYNGAP1 suppresses the proliferation of rectal adenocarcinoma via Wnt/β-Catenin signaling pathway

Xiao,

Zhu,

Chen

et al. 2024

Discov Onc

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Rectal adenocarcinoma (READ) is a common malignant tumor of the digestive tract. Growing studies have confirmed Ras GTPase-activating proteins are involved in the progression of several tumors. This study aimed to explore the expression and function of Ras GTPase-activating proteins in READ. In this study, we analyzed RNA sequencing data from 165 patients with READ and 789 normal tissue samples, identifying 5603 differentially expressed genes (DEGs), including 2937 upregulated genes and 2666 downregulated genes. Moreover, we also identified two dysregulated genes, RASA4 and SYNGAP1, among six Ras GTPase-activating proteins. High NF1 expression was associated with longer overall survival, while high SYNGAP1 expression showed a trend towards extended overall survival. Further analysis revealed the mutation frequency and copy number variations of Ras GTPase-activating proteins in various cancer samples. Additionally, DNA methylation analysis demonstrated a negative correlation between DNA methylation of Ras GTPase-activating proteins and their expression. Moreover, among Ras GTPase-activating proteins, we focused on SYNGAP1, and experimental validation confirmed that the overexpression of SYNGAP1 in READ significantly suppressed READ cell proliferation and increased apoptosis via regulating the Wnt/β-Catenin signaling pathway. These findings underscored the potential significance of SYNGAP1 in READ and provide new insights for further research and treatment.

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“…Wnt is a regulator of EMT and it induces EMT in increasing tumor progression. A high expression level of Wnt occurs during the progression of tumor cells and promotes metastasis [16].…”

Section: Discussionmentioning

confidence: 99%

Identification of Genes Crucial for Biological Processes in Breast Cancer Liver Metastasis Relapse

Kwok,

Yeguvapalli,

Chitrala

2024

IJMS

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Breast cancer, when advancing to a metastatic stage, involves the liver, impacting over 50% of cases and significantly diminishing survival rates. Presently, a lack of tailored therapeutic protocols for breast cancer liver metastasis (BCLM) underscores the need for a deeper understanding of molecular patterns governing this complication. Therefore, by analyzing differentially expressed genes (DEGs) between primary breast tumors and BCLM lesions, we aimed to shed light on the diversities of this process. This research investigated breast cancer liver metastasis relapse by employing a comprehensive approach that integrated data filtering, gene ontology and KEGG pathway analysis, overall survival analysis, identification of the alteration in the DEGs, visualization of the protein–protein interaction network, Signor 2.0, identification of positively correlated genes, immune cell infiltration analysis, genetic alternation analysis, copy number variant analysis, gene-to-mRNA interaction, transcription factor analysis, molecular docking, and identification of potential treatment targets. This study’s integrative approach unveiled metabolic reprogramming, suggesting altered PCK1 and LPL expression as key in breast cancer metastasis recurrence.

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Wnt/β-catenin-driven EMT regulation in human cancers

Cited by 22 publications

References 225 publications

The ERK1/2-Elk1, JNK-cJun, and JAK-STAT Transcriptional Axes as Potential Bortezomib Resistance Mediators in Prostate Cancer

The ERK1/2-Elk1, JNK-cJun, and JAK-STAT Transcriptional Axes as Potential Bortezomib Resistance Mediators in Prostate Cancer

Overexpression of SYNGAP1 suppresses the proliferation of rectal adenocarcinoma via Wnt/β-Catenin signaling pathway

Identification of Genes Crucial for Biological Processes in Breast Cancer Liver Metastasis Relapse

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