Download full-text PDF

Source
http://dx.doi.org/10.1111/pcmr.12249DOI Listing

Publication Analysis

Top Keywords

melanoma hippo
4
hippo signaling
4
signaling copy
4
copy number
4
number alterations
4
alterations yap1
4
yap1 overexpression
4
overexpression impairs
4
impairs patient
4
patient survival
4

Similar Publications

Genotype-informed anticancer therapies such as BRAF inhibitors can show remarkable clinical efficacy in BRAF-mutant melanoma; however, drug resistance poses a major hurdle to successful cancer treatment. Many resistance events to targeted therapies have been identified, suggesting a complex path to improve therapeutics. Here, we showed the utility of a piggyBac transposon activation mutagenesis screen for the efficient identification of genes that are resistant to BRAF inhibition in melanoma.

View Article and Find Full Text PDF

: With the rise in prevalence of diagnostic genetic techniques like RNA sequencing and whole exome sequencing (WES), as well as biological treatment regiments for cancer therapy, several genes have been implicated in carcinogenesis. This review aims to update our understanding of the Neurofibromatosis 2 (NF2) gene and its role in the pathogenesis of various cancers. : A comprehensive search of five online databases yielded 43 studies that highlighted the effect of sporadic NF2 mutations on several cancers, including sporadic meningioma, ependymoma, schwannoma, mesothelioma, breast cancer, hepatocellular carcinoma, prostate cancer, glioblastoma, thyroid cancer, and melanoma.

View Article and Find Full Text PDF

Pannexin 1 crosstalk with the Hippo pathway in malignant melanoma.

FEBS J

January 2025

Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Canada.

In this study, we explored the intricate relationship between Pannexin 1 (PANX1) and the Hippo signaling pathway effector, Yes-associated protein (YAP). Analysis of The Cancer Genome Atlas (TCGA) data revealed a significant positive correlation between PANX1 mRNA and core Hippo components, Yes-associated protein 1 [YAP], Transcriptional coactivator with PDZ-binding motif [TAZ], and Hippo scaffold, Ras GTPase-activating-like protein IQGAP1 [IQGAP1], in invasive cutaneous melanoma and breast carcinoma. Furthermore, we demonstrated that PANX1 expression is upregulated in invasive melanoma cell lines and is associated with increased YAP protein levels.

View Article and Find Full Text PDF
Article Synopsis
  • Melanoma is a highly aggressive cancer that bypasses key signaling pathways, specifically MAPK and Hippo, with the review focusing on the role of STK3 in the Hippo pathway for potential treatments.
  • The study covers the interaction of STK3 with the MAPK/ERK pathway, emphasizing its functions in promoting cancer cell death (apoptosis), halting tumor growth, and controlling metastasis as a tumor suppressor.
  • Targeting STK3 can involve strategies like activating it directly, inhibiting its downstream effectors such as YAP/TAZ, or combining treatments with existing BRAF inhibitors, but challenges in developing STK3-targeted drugs remain.
View Article and Find Full Text PDF

PDE4D drives rewiring of the MAPK pathway in BRAF-mutated melanoma resistant to MAPK inhibitors.

Cell Commun Signal

November 2024

Human Immunology Pathophysiology & Immunotherapy (HIPI), Université Paris Cité, INSERM U976 - Hôpital Saint Louis - 1 avenue Claude Vellefaux, Paris, 75010, France.

Background: Phosphodiesterase type 4D (PDE4D) breaks down cyclic AMP (cAMP) reducing the signaling of this intracellular second messenger which plays a major role in melanocyte pathophysiology. In advanced melanoma, expression of PDE4D is increased, plays a role in tumor invasion and is negatively associated with survival. In the current work, we investigated the role of PDE4D in the resistance of BRAF-mutated melanoma to mitogen-activated protein kinase (MAPK) pathway-targeted therapy.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!