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Cancers
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YAP (Yes-Associated Protein) in Cancer
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YAP (Yes-Associated Protein) in Cancer

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

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 16852

Special Issue Editors

Dr. Alessandra Marchetti

E-Mail Website
Guest Editor
Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy
Interests: hepatocellular carcinoma/HCC; tumor suppression; EMT; signal transduction; hepatocyte differentiation; tumor microenvironment
Dr. Laura Amicone

E-Mail Website
Guest Editor
Department of Molecular Medicine, Sapienza University of Rome, Piazzale Aldo Moro, 5, 00185 Roma RM, Italy
Interests: liver cell stemness; EMT/MET in liver cells; molecular and epigenetic control of liver functions; mechanical control of liver cell differentiation/function

Special Issue Information

Dear Colleagues,

The Yes-associated protein (YAP) is a highly evolutionarily conserved transcriptional co-factor involved, mainly together with the transcriptional coactivator with PDZ-binding motif (TAZ), in the regulation of various cellular processes, including proliferation, survival, differentiation, and stem cell maintenance. Dysregulation of YAP expression/activity has been frequently observed in cancer, where it plays a pivotal role in both tumor onset and progression. While oncogenic YAP activity has been widely reported, recent data unveiled a tumor suppressor role in specific cellular contexts. Moreover, additional roles of YAP in inflammation and tumor immunity have been described, indicating the protein as a key inducer of tumor microenvironmental changes.

YAP is the downstream effector of several diffusible and/or mechanical extracellular stimuli that are transduced by multiple molecular signaling pathways, mainly converging on the inhibitory Hippo pathway. Chemical compounds directly targeting inappropriate YAP transcriptional activity or YAP-regulating signaling pathways have been developed and successfully tested in preclinical models for their capability to interfere with tumor growth and progression. However, their further characterization in terms of specificity and toxicity in vivo is required.

An advance in the development of multitargeting strategies for cancer treatment can be provided only by dissecting the complexity of YAP function and regulation. Therefore, a deeper characterization of YAP extracellular inducers and intracellular regulators, as well as the impact of YAP activity on cancer cells and tumor microenvironment, needs to be addressed. This Special Issue will highlight the role of YAP and of its complex regulation in cancer, through both basic and preclinical studies, thus opening new perspectives for targeted therapies.

Dr. Alessandra Marchetti
Prof. Laura Amicone
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.

Keywords

  • YAP/TAZ
  • Hippo pathway
  • Tumor microenvironment
  • Mechanotransduction
  • Signaling pathways
  • Stemness/differentiation
  • Targeted therapy

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Published Papers (4 papers)

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Research

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15 pages, 2687 KiB  
Article
NPFFR2 Contributes to the Malignancy of Hepatocellular Carcinoma Development by Activating RhoA/YAP Signaling
by Yuna Shin, Wonhee Jung, Mi-Yeon Kim, Dongjo Shin, Geun Hee Kim, Chun Ho Kim, Sun-Hoo Park, Eung-Ho Cho, Dong Wook Choi, Chul Ju Han, Kee Ho Lee, Sang-Bum Kim and Hyun Jin Shin
Cancers 2022, 14(23), 5850; https://doi.org/10.3390/cancers14235850 - 27 Nov 2022
Cited by 4 | Viewed by 2222
Abstract
G protein–coupled receptors (GPCRs) are a diverse family of cell surface receptors implicated in various physiological functions, making them common targets for approved drugs. Many GPCRs are abnormally activated in cancers and have emerged as therapeutic targets for cancer. Neuropeptide FF receptor 2 [...] Read more.
G protein–coupled receptors (GPCRs) are a diverse family of cell surface receptors implicated in various physiological functions, making them common targets for approved drugs. Many GPCRs are abnormally activated in cancers and have emerged as therapeutic targets for cancer. Neuropeptide FF receptor 2 (NPFFR2) is a GPCR that helps regulate pain and modulates the opioid system; however, its function remains unknown in cancers. Here, we found that NPFFR2 is significantly up-regulated in liver cancer and its expression is related to poor prognosis. Silencing of NPFFR2 reduced the malignancy of liver cancer cells by decreasing cell survival, invasion, and migration, while its overexpression increased invasion, migration, and anchorage-independent cell growth. Moreover, we found that the malignant function of NPFFR2 depends on RhoA and YAP signaling. Inhibition of Rho kinase activity completely restored the phenotypes induced by NPFFR2, and RhoA/F-Actin/YAP signaling was controlled by NPFFR2. These findings demonstrate that NPFFR2 may be a potential target for the treatment of hepatocellular carcinoma. Full article
(This article belongs to the Special Issue YAP (Yes-Associated Protein) in Cancer)
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Review

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32 pages, 4143 KiB  
Review
Emerging Principles in the Transcriptional Control by YAP and TAZ
by Alejandro Lopez-Hernandez, Silvia Sberna and Stefano Campaner
Cancers 2021, 13(16), 4242; https://doi.org/10.3390/cancers13164242 - 23 Aug 2021
Cited by 28 | Viewed by 5327
Abstract
Yes-associated protein (YAP) and TAZ are transcriptional cofactors that sit at the crossroad of several signaling pathways involved in cell growth and differentiation. As such, they play essential functions during embryonic development, regeneration, and, once deregulated, in cancer progression. In this review, we [...] Read more.
Yes-associated protein (YAP) and TAZ are transcriptional cofactors that sit at the crossroad of several signaling pathways involved in cell growth and differentiation. As such, they play essential functions during embryonic development, regeneration, and, once deregulated, in cancer progression. In this review, we will revise the current literature and provide an overview of how YAP/TAZ control transcription. We will focus on data concerning the modulation of the basal transcriptional machinery, their ability to epigenetically remodel the enhancer–promoter landscape, and the mechanisms used to integrate transcriptional cues from multiple pathways. This reveals how YAP/TAZ activation in cancer cells leads to extensive transcriptional control that spans several hallmarks of cancer. The definition of the molecular mechanism of transcriptional control and the identification of the pathways regulated by YAP/TAZ may provide therapeutic opportunities for the effective treatment of YAP/TAZ-driven tumors. Full article
(This article belongs to the Special Issue YAP (Yes-Associated Protein) in Cancer)
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27 pages, 1664 KiB  
Review
An Updated Understanding of the Role of YAP in Driving Oncogenic Responses
by Giampaolo Morciano, Bianca Vezzani, Sonia Missiroli, Caterina Boncompagni, Paolo Pinton and Carlotta Giorgi
Cancers 2021, 13(12), 3100; https://doi.org/10.3390/cancers13123100 - 21 Jun 2021
Cited by 17 | Viewed by 4582
Abstract
Yes-associated protein (YAP) has emerged as a key component in cancer signaling and is considered a potent oncogene. As such, nuclear YAP participates in complex and only partially understood molecular cascades that are responsible for the oncogenic response by regulating multiple processes, including [...] Read more.
Yes-associated protein (YAP) has emerged as a key component in cancer signaling and is considered a potent oncogene. As such, nuclear YAP participates in complex and only partially understood molecular cascades that are responsible for the oncogenic response by regulating multiple processes, including cell transformation, tumor growth, migration, and metastasis, and by acting as an important mediator of immune and cancer cell interactions. YAP is finely regulated at multiple levels, and its localization in cells in terms of cytoplasm–nucleus shuttling (and vice versa) sheds light on interesting novel anticancer treatment opportunities and putative unconventional functions of the protein when retained in the cytosol. This review aims to summarize and present the state of the art knowledge about the role of YAP in cancer signaling, first focusing on how YAP differs from WW domain-containing transcription regulator 1 (WWTR1, also named as TAZ) and which upstream factors regulate it; then, this review focuses on the role of YAP in different cancer stages and in the crosstalk between immune and cancer cells as well as growing translational strategies derived from its inhibitory and synergistic effects with existing chemo-, immuno- and radiotherapies. Full article
(This article belongs to the Special Issue YAP (Yes-Associated Protein) in Cancer)
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26 pages, 949 KiB  
Review
New Insights into YES-Associated Protein Signaling Pathways in Hematological Malignancies: Diagnostic and Therapeutic Challenges
by Alessandro Allegra, Giovanni Pioggia, Vanessa Innao, Caterina Musolino and Sebastiano Gangemi
Cancers 2021, 13(8), 1981; https://doi.org/10.3390/cancers13081981 - 20 Apr 2021
Cited by 17 | Viewed by 3813
Abstract
The Hippo/YES-associated protein (YAP) signaling pathway is a cell survival and proliferation-control system with its main activity that of regulating cell growth and organ volume. YAP operates as a transcriptional coactivator in regulating the onset, progression, and treatment response in numerous human tumors. [...] Read more.
The Hippo/YES-associated protein (YAP) signaling pathway is a cell survival and proliferation-control system with its main activity that of regulating cell growth and organ volume. YAP operates as a transcriptional coactivator in regulating the onset, progression, and treatment response in numerous human tumors. Moreover, there is evidence suggesting the involvement of YAP in the control of the hematopoietic system, in physiological conditions rather than in hematological diseases. Nevertheless, several reports have proposed that the effects of YAP in tumor cells are cell-dependent and cell-type-determined, even if YAP usually interrelates with extracellular signaling to stimulate the onset and progression of tumors. In the present review, we report the most recent findings in the literature on the relationship between the YAP system and hematological neoplasms. Moreover, we evaluate the possible therapeutic use of the modulation of the YAP system in the treatment of malignancies. Given the effects of the YAP system in immunosurveillance, tumorigenesis, and chemoresistance, further studies on interactions between the YAP system and hematological malignancies will offer very relevant information for the targeting of these diseases employing YAP modifiers alone or in combination with chemotherapy drugs. Full article
(This article belongs to the Special Issue YAP (Yes-Associated Protein) in Cancer)
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