Review
Cell Biology
Ishita S. Hiremath, Arul Goel, Sudha Warrier, Alan Prem Kumar, Gautam Sethi, Manoj Garg
Summary: The Wnt/β-catenin signaling pathway is crucial for various physiological processes and implicated in the development of several cancers. Different regulators of the pathway play essential roles in cancer development.
JOURNAL OF CELLULAR PHYSIOLOGY
(2022)
Article
Multidisciplinary Sciences
Line Mygland, Shoshy Alam Brinch, Martin Frank Strand, Petter Angell Olsen, Aleksandra Aizenshtadt, Kaja Lund, Nina Therese Solberg, Max Lycke, Tor Espen Thorvaldsen, Sandra Espada, Dorna Misaghian, Christian M. Page, Oleg Agafonov, Stale Nygard, Nai-Wen Chi, Eva Lin, Jenille Tan, Yihong Yu, Mike Costa, Stefan Krauss, Jo Waaler
Summary: Small-molecule tankyrase 1 and tankyrase 2 (TNKS1/2) inhibitors have shown to be effective antitumor agents in specific tumor cell lines, with the ability to inhibit key signaling pathways and reduce expression of crucial oncogenes, ultimately impairing cell growth. Additionally, these inhibitors induce the accumulation of beta-catenin degradasomes containing TNKS1/2, which interact with YAP and angiomotin proteins, leading to attenuation of YAP signaling. Further research is needed to fully evaluate the potential of TNKS inhibitors in cancer treatment.
Review
Biochemistry & Molecular Biology
Qiyun Xiao, Johannes Werner, Nachiyappan Venkatachalam, Kim E. Boonekamp, Matthias P. Ebert, Tianzuo Zhan
Summary: Targeting cancer hallmarks is crucial for improving anti-cancer treatment, but cross-talk between signaling pathways often leads to resistance. This article provides an overview of the molecular interactions between the p53 and Wnt pathways in cancer, including complex feedback loops and reciprocal transactivation, as well as the mutational landscape of genes associated with these pathways.
Article
Biochemistry & Molecular Biology
Yuri Lee, Hai-long Piao, Jongchan Kim
Summary: The Wnt signaling pathway is crucial for regulating various cellular processes, and dysregulation of this pathway has been linked to human diseases, including cancer. In this study, researchers aimed to identify the deubiquitinases (DUBs) that regulate the pathway through the essential component LEF1. They discovered that OTUD7B interacts with LEF1 and activates Wnt signaling. Furthermore, OTUD7B promotes the nuclear localization of LEF1, leading to increased interaction with beta-catenin. This study suggests that OTUD7B may serve as a potential therapeutic target in diseases where Wnt signaling is dysregulated, such as cancer.
Article
Oncology
Kathleen A. O'Leary, Debra E. Rugowski, Michael P. Shea, Ruth Sullivan, Amy R. Moser, Linda A. Schuler
Summary: Prolactin (PRL) collaborates with Apc(Min/+) to increase tumor incidence and modulate cancer stem cell activity through Notch-driven signals, shedding light on mechanisms whereby PRL elevates risk of breast cancer.
Article
Oncology
Yang Zhou, Jiang Xu, Haichang Luo, Xiangjing Meng, Ming Chen, Di Zhu
Summary: Abnormal activation of the Wnt/beta-catenin signaling pathway is closely related to tumorigenesis and immune surveillance, leading to increased resistance to immunotherapy.
Article
Multidisciplinary Sciences
Ana R. Moshkovsky, Marc W. Kirschner
Summary: Axin is a crucial protein in the canonical Wnt pathway, and its differential regulation allows for tissue-specific functions.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2022)
Review
Biochemistry & Molecular Biology
Sarah Koushyar, Valerie S. Meniel, Toby J. Phesse, Helen B. Pearson
Summary: Aberrant activation of the Wnt pathway is closely related to tumor formation, progression, and therapeutic resistance in prostate cancer. Targeting the Wnt pathway for prostate cancer treatment has shown potential efficacy. However, the functional consequences of activating the Wnt pathway during different stages of prostate cancer progression are still unclear. Preclinical research on targeting Wnt signaling in the treatment of prostate cancer is crucial for identifying effective treatment strategies and improving patient care.
Review
Cell Biology
Chenchen Li, Emma E. Furth, Anil K. Rustgi, Peter S. Klein
Summary: The Wnt signaling pathway is crucial in metazoan development and stem cell maintenance, and is also involved in various malignancies. Apart from the canonical activation, the pathway can affect cell function through multiple alternative effectors, potentially contributing to cancer development.
Article
Multidisciplinary Sciences
Chen Shen, Anmada Nayak, Leif R. Neitzel, Amber A. Adams, Maya Silver-Isenstadt, Leah M. Sawyer, Hassina Benchabane, Huilan Wang, Nawat Bunnag, Bin Li, Daniel T. Wynn, Fan Yang, Marta Garcia-Contreras, Charles H. Williams, Sivanesan Dakshanamurthy, Charles C. Hong, Nagi G. Ayad, Anthony J. Capobianco, Yashi Ahmed, Ethan Lee, David J. Robbins
Summary: This study reveals how the Wnt ligand can enhance CRBN-dependent protein degradation and highlights the importance of CRBN in physiological Wnt signaling.
NATURE COMMUNICATIONS
(2021)
Article
Biochemistry & Molecular Biology
Mingliang He, Xiaoyang Lv, Xiukai Cao, Zehu Yuan, Tesfaye Getachew, Yutao Li, Shanhe Wang, Wei Sun
Summary: SRY-box transcription factor 18 (SOX18) is expressed in dermal papilla cells (DPCs) of sheep hair follicles and plays a crucial role in promoting DPC proliferation through activating the Wnt/β-Catenin signaling pathway. Inhibition of the Wnt/β-Catenin signaling pathway can be rescued by SOX18, suggesting the essential role of SOX18 in governing DPC proliferation and hair growth.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Medicine, Research & Experimental
Zheng Qin, Yupei Li, Jiameng Li, Luojia Jiang, Zhuyun Zhang, Kaixi Chang, Qinbo Yang, Shanshan Chen, Ruoxi Liao, Baihai Su
Summary: This study found that exosomal STAT1 derived from HP-treated HUVECs can promote VSMC calcification. Activation of the Wnt/beta-catenin pathway may be a potential mechanism of exosome-promoted VSMC calcification.
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
(2022)
Review
Biochemistry & Molecular Biology
Xinbing Yang, Yajing Du, Lulu Luo, Xinru Xu, Shizheng Xiong, Xueni Yang, Li Guo, Tingming Liang
Summary: Dysregulated expression of specific non-coding RNAs (ncRNAs) has been strongly linked to tumorigenesis, cancer progression, and therapeutic resistance. Recent evidence suggests that ncRNAs can interact with the Wnt/beta-catenin signaling pathway, influencing the expression of Wnt target genes in cancer cells. This review aims to unravel the complex associations between ncRNAs and the Wnt/beta-catenin signaling pathway and explore their potential implications for cancer therapy.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Xiaobin Shang, Kai Oliver Boeker, Shahed Taheri, Thelonius Hawellek, Wolfgang Lehmann, Arndt F. Schilling
Summary: Osteoarthritis is a chronic disease that lacks disease-modifying treatment, with the Wnt/beta-catenin pathway playing a key role in its pathophysiology. Both excessive stimulation and suppression of this pathway can contribute to the development of OA. MicroRNAs have been found to regulate various cellular processes in different diseases, offering potential insights for the development of miRNA-based therapeutics for OA.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Cell Biology
Wibke Groenewald, Anders H. H. Lund, David Michael Gay
Summary: It is well known that mutations in the WNT-signalling pathway are significant in cancer development. Understanding the role and occurrence of these mutations within the pathway is crucial for developing effective therapeutic strategies. Some cancers have mutations at the receptor level of the pathway, while others have mutations in the cytoplasmic segment, leading to ligand-dependent or ligand-independent pathway activation, respectively. This review explores the driving mutations in cancer and the available therapeutic interventions for each type of mutation, and also discusses a potential new therapeutic avenue targeting the translational apparatus downstream from WNT signalling.