Wnt Signaling Pathways in Keratinocyte Carcinomas

Lang, Christopher; Chan, Chim Kei; Veltri, Anthony; Lien, Wen-Hui

doi:10.3390/cancers11091216

Cited by 31 publications

(19 citation statements)

References 196 publications

(226 reference statements)

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“…CaN via dephosphorylation activates nuclear factor of activated T-cells (NFAT) that translocates to the nucleus and regulates the expression of target genes. WNT/Ca 2+ pathway activation plays an important role in the regulation of cell motility and cytoskeleton organization [17,54,55].…”

Section: Non-canonical Wnt Signalingmentioning

confidence: 99%

WNT Signaling in Melanoma

Gajos-Michniewicz

Czyż

2020

IJMS

145

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WNT-signaling controls important cellular processes throughout embryonic development and adult life, so any deregulation of this signaling can result in a wide range of pathologies, including cancer. WNT-signaling is classified into two categories: β-catenin-dependent signaling (canonical pathway) and β-catenin-independent signaling (non-canonical pathway), the latter can be further divided into WNT/planar cell polarity (PCP) and calcium pathways. WNT ligands are considered as unique directional growth factors that contribute to both cell proliferation and polarity. Origin of cancer can be diverse and therefore tissue-specific differences can be found in WNT-signaling between cancers, including specific mutations contributing to cancer development. This review focuses on the role of the WNT-signaling pathway in melanoma. The current view on the role of WNT-signaling in cancer immunity as well as a short summary of WNT pathway-related drugs under investigation are also provided.

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Section: Non-canonical Wnt Signalingmentioning

confidence: 99%

WNT Signaling in Melanoma

Gajos-Michniewicz

Czyż

2020

IJMS

145

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“…In the presence of VacA, GSK3β is inactivated and leads to the accumulation of β-catenin in the cytoplasm [86]. The β-catenin enters the nucleus where it acts as a coactivator TCF (T cell factor) and LEF (lymphoid enhancer factor) transcription factor for activating transcription of β-catenin-dependent genes such as cyclin D1 [67,87]. Overexpression of cyclin D1 is associated with cancers in humans [88] (Fig.…”

Section: Vacuolating Cytotoxin a And Gastric Cancermentioning

confidence: 99%

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Alipour

2020

J Gastrointest Canc

153

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Introduction Various types of cancers threaten human life. The role of bacteria in causing cancer is controversial, but it has been determined that the Helicobacter pylori infection is one of the identified risk factors for gastric cancer. Helicobacter pylori infection is highly prevalent, and about half of the world , s population is infected with it. Objective The aim of this study was the role of Helicobacter pylori in the development of gastric cancer. Method We obtained information from previously published articles. Results and Conclusion The bacterium has various virulence factors, including cytotoxin-associated gene A, vacuolating cytotoxin A, and the different outer membrane proteins that cause cancer by different mechanisms. These virulence factors activate cell signaling pathways such as PI3-kinase/Akt, JAK/STAT and Ras, Raf, and ERK signaling that control cell proliferation. Uncontrolled proliferation can lead to cancer.

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“…The Wnt signaling pathway may be activated by the Wnt/ß-catenin pathway (also known as the canonical pathway ( Figure 1 ) ( 185 , 186 ) or non-canonical Wnt signaling. Non-canonical Wnt signaling, which is independent of β-catenin, is activated by the pathways Wnt/planar cell polarity and Wnt/Ca 2+ ( 187 , 188 ).…”

Section: Regulation Of Wnt Canonical and Non-canonical Pathways By Dnmentioning

confidence: 99%

Role of DNA Methylation in the Resistance to Therapy in Solid Tumors

Romero-García¹,

Prado-Garcı́a²,

Carlos‐Reyes³

2020

Front. Oncol.

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Despite the recent advances in chemotherapeutic treatments against cancer, some types of highly aggressive and invasive cancer develop drug resistance against conventional therapies, which continues to be a major problem in the fight against cancer. In recent years, studies of alterations of DNA methylome have given us a better understanding of the role of DNA methylation in the development of tumors. DNA methylation (DNAm) is an epigenetic change that promotes the covalent transfer of methyl groups to DNA. This process suppresses gene expression through the modulation of the transcription machinery access to the chromatin or through the recruitment of methyl binding proteins. DNAm is regulated mainly by DNA methyltransferases. Aberrant DNAm contributes to tumor progression, metastasis, and resistance to current anti-tumoral therapies. Aberrant DNAm may occur through hypermethylation in the promoter regions of tumor suppressor genes, which leads to their silencing, while hypomethylation in the promoter regions of oncogenes can activate them. In this review, we discuss the impact of dysregulated methylation in certain genes, which impact signaling pathways associated with apoptosis avoidance, metastasis, and resistance to therapy. The analysis of methylome has revealed patterns of global methylation, which regulate important signaling pathways involved in therapy resistance in different cancer types, such as breast, colon, and lung cancer, among other solid tumors. This analysis has provided gene-expression signatures of methylated region-specific DNA that can be used to predict the treatment outcome in response to anti-cancer therapy. Additionally, changes in cancer methylome have been associated with the acquisition of drug resistance. We also review treatments with demethylating agents that, in combination with standard therapies, seem to be encouraging, as tumors that are in early stages can be successfully treated. On the other hand, tumors that are in advanced stages can be treated with these combination schemes, which could sensitize tumor cells that are resistant to the therapy. We propose that rational strategies, which combine specific demethylating agents with conventional treatment, may improve overall survival in cancer patients.

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Wnt Signaling Pathways in Keratinocyte Carcinomas

Cited by 31 publications

References 196 publications

WNT Signaling in Melanoma

WNT Signaling in Melanoma

Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer

Role of DNA Methylation in the Resistance to Therapy in Solid Tumors

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