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Cancers
Special Issues
Hippo Signaling in Cancer
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Hippo Signaling in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (20 February 2024) | Viewed by 3523

Special Issue Editors

Dr. Ying Yan

E-Mail Website
Guest Editor
Department of Radiation Oncology, College of Medicine, University of Nebraska Medical Center, Omaha, NE, USA
Interests: Hippo; AKT1; phosphorylation; radiation; DSB
Prof. Dr. Michel Ouellette

E-Mail Website
Guest Editor
Department of Internal Medicine, College of Medicine, University of Nebraska Medical Center, Omaha, NE, USA
Interests: Hippo; pancreatic cancer; telomeres/telomerase; Rac1, GTPase, and K-ras signaling

Special Issue Information

Dear Colleagues,

This Special Issue in Cancers aims to present the current achievements of scientific investigations focusing on Hippo signaling, with emphasis on oncogenesis, cancer progression, metastasis, cancer therapy resistance, and the development of targeted anticancer agents based on Hippo signaling. The topic is of particular importance because the dysregulation of Hippo signaling occurs in many types of human cancer and contributes to cancer development, progression, metastasis, and therapeutic resistance. Recent advances in methods and technologies of cell biology, molecular biology, immunology, and biochemistry have enabled fast growth in this area. This Special Issue aims to present the most important recent achievements in this unique field of cancer research. 

Dr. Ying Yan
Prof. Dr. Michel Ouellette
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

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Published Papers (3 papers)

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Research

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24 pages, 3073 KiB  
Article
Rac1 GTPase Regulates the βTrCP-Mediated Proteolysis of YAP Independently of the LATS1/2 Kinases
by Chitra Palanivel, Tabbatha N. Somers, Bailey M. Gabler, Yuanhong Chen, Yongji Zeng, Jesse L. Cox, Parthasarathy Seshacharyulu, Jixin Dong, Ying Yan, Surinder K. Batra and Michel M. Ouellette
Cancers 2024, 16(21), 3605; https://doi.org/10.3390/cancers16213605 - 25 Oct 2024
Viewed by 636
Abstract
Background: Oncogenic mutations in the KRAS gene are detected in >90% of pancreatic cancers (PC). In genetically engineered mouse models of PC, oncogenic KRAS drives the formation of precursor lesions and their progression to invasive PC. The Yes-associated Protein (YAP) is a transcriptional [...] Read more.
Background: Oncogenic mutations in the KRAS gene are detected in >90% of pancreatic cancers (PC). In genetically engineered mouse models of PC, oncogenic KRAS drives the formation of precursor lesions and their progression to invasive PC. The Yes-associated Protein (YAP) is a transcriptional coactivator required for transformation by the RAS oncogenes and the development of PC. In Ras-driven tumors, YAP can also substitute for oncogenic KRAS to drive tumor survival after the repression of the oncogene. Ras oncoproteins exert their transforming properties through their downstream effectors, including the PI3K kinase, Rac1 GTPase, and MAPK pathways. Methods: To identify Ras effectors that regulate YAP, YAP levels were measured in PC cells exposed to inhibitors of oncogenic K-Ras and its effectors. Results: In PC cells, the inhibition of Rac1 leads to a time-dependent decline in YAP protein, which could be blocked by proteosome inhibitor MG132. This YAP degradation after Rac1 inhibition was observed in a range of cell lines using different Rac1 inhibitors, Rac1 siRNA, or expression of dominant negative Rac1T17N mutant. Several E3 ubiquitin ligases, including SCFβTrCP, regulate YAP protein stability. To be recognized by this ligase, the βTrCP degron of YAP (amino acid 383–388) requires its phosphorylation by casein kinase 1 at Ser384 and Ser387, but these events must first be primed by the phosphorylation of Ser381 by LATS1/2. Using Flag-tagged mutants of YAP, we show that YAP degradation after Rac1 inhibition requires the integrity of this degron and is blocked by the silencing of βTrCP1/2 and by the inhibition of casein kinase 1. Unexpectedly, YAP degradation after Rac1 inhibition was still observed after the silencing of LATS1/2 or in cells carrying a LATS1/2 double knockout. Conclusions: These results reveal Rac1 as an oncogenic KRAS effector that contributes to YAP stabilization in PC cells. They also show that this regulation of YAP by Rac1 requires the SCFβTrCP ligase but occurs independently of the LATS1/2 kinases. Full article
(This article belongs to the Special Issue Hippo Signaling in Cancer)
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35 pages, 7506 KiB  
Article
The Interaction of Mechanics and the Hippo Pathway in Drosophila melanogaster
by Jia Gou, Tianhao Zhang and Hans G. Othmer
Cancers 2023, 15(19), 4840; https://doi.org/10.3390/cancers15194840 - 3 Oct 2023
Viewed by 1459
Abstract
Drosophila melanogaster has emerged as an ideal system for studying the networks that control tissue development and homeostasis and, given the similarity of the pathways involved, controlled and uncontrolled growth in mammalian systems. The signaling pathways used in patterning the Drosophila wing disc [...] Read more.
Drosophila melanogaster has emerged as an ideal system for studying the networks that control tissue development and homeostasis and, given the similarity of the pathways involved, controlled and uncontrolled growth in mammalian systems. The signaling pathways used in patterning the Drosophila wing disc are well known and result in the emergence of interaction of these pathways with the Hippo signaling pathway, which plays a central role in controlling cell proliferation and apoptosis. Mechanical effects are another major factor in the control of growth, but far less is known about how they exert their control. Herein, we develop a mathematical model that integrates the mechanical interactions between cells, which occur via adherens and tight junctions, with the intracellular actin network and the Hippo pathway so as to better understand cell-autonomous and non-autonomous control of growth in response to mechanical forces. Full article
(This article belongs to the Special Issue Hippo Signaling in Cancer)
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Review

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15 pages, 1924 KiB  
Review
Regulation of Tumor Microenvironment through YAP/TAZ under Tumor Hypoxia
by Sung Hoon Choi and Do Young Kim
Cancers 2024, 16(17), 3030; https://doi.org/10.3390/cancers16173030 - 30 Aug 2024
Viewed by 848
Abstract
In solid tumors such as hepatocellular carcinoma (HCC), hypoxia is one of the important mechanisms of cancer development that closely influences cancer development, survival, and metastasis. The development of treatments for cancer was temporarily revolutionized by immunotherapy but continues to be constrained by [...] Read more.
In solid tumors such as hepatocellular carcinoma (HCC), hypoxia is one of the important mechanisms of cancer development that closely influences cancer development, survival, and metastasis. The development of treatments for cancer was temporarily revolutionized by immunotherapy but continues to be constrained by limited response rates and the resistance and high costs required for the development of new and innovative strategies. In particular, solid tumors, including HCC, a multi-vascular tumor type, are sensitive to hypoxia and generate many blood vessels for metastasis and development, making it difficult to treat HCC, not only with immunotherapy but also with drugs targeting blood vessels. Therefore, in order to develop a treatment strategy for hypoxic tumors, various mechanisms must be explored and analyzed to treat these impregnable solid tumors. To date, tumor growth mechanisms linked to hypoxia are known to be complex and coexist with various signal pathways, but recently, mechanisms related to the Hippo signal pathway are emerging. Interestingly, Hippo YAP/TAZ, which appear during early tumor and normal tumor growth, and YAP/TAZ, which appear during hypoxia, help tumor growth and proliferation in different directions. Peculiarly, YAP/TAZ, which have different phosphorylation directions in the hypoxic environment of tumors, are involved in cancer proliferation and metastasis in various carcinomas, including HCC. Analyzing the mechanisms that regulate the function and expression of YAP in addition to HIF in the complex hypoxic environment of tumors may lead to a variety of anti-cancer strategies and combining HIF and YAP/TAZ may develop the potential to change the landscape of cancer treatment. Full article
(This article belongs to the Special Issue Hippo Signaling in Cancer)
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