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Article: Regulation of NFκB Signalling by Ubiquitination: A Potential Therapeutic Target in Head and Neck Squamous Cell Carcinoma?

Morgan, Ethan L / Chen, Zhong / Van Waes, Carter

2020 Volume 12, Issue 10

Abstract: Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, with over 600,000 cases per year. The primary causes for HNSCC include smoking and alcohol consumption, with an increasing number of cases attributed to infection ... ...

Abstract	Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, with over 600,000 cases per year. The primary causes for HNSCC include smoking and alcohol consumption, with an increasing number of cases attributed to infection with Human Papillomavirus (HPV). The treatment options for HNSCC currently include surgery, radiotherapy, and/or platinum-based chemotherapeutics. Cetuximab (targeting EGFR) and Pembrolizumab (targeting PD-1) have been approved for advanced stage, recurrent, and/or metastatic HNSCC. Despite these advances, whilst HPV+ HNSCC has a 3-year overall survival (OS) rate of around 80%, the 3-year OS for HPV- HNSCC is still around 55%. Aberrant signal activation of transcription factor NFκB plays an important role in the pathogenesis and therapeutic resistance of HNSCC. As an important mediator of inflammatory signalling and the immune response to pathogens, the NFκB pathway is tightly regulated to prevent chronic inflammation, a key driver of tumorigenesis. Here, we discuss how NFκB signalling is regulated by the ubiquitin pathway and how this pathway is deregulated in HNSCC. Finally, we discuss the current strategies available to target the ubiquitin pathway and how this may offer a potential therapeutic benefit in HNSCC.
Language	English
Publishing date	2020-10-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12102877
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Genomics and advances towards precision medicine for head and neck squamous cell carcinoma.

Van Waes, Carter / Musbahi, Omar

Laryngoscope investigative otolaryngology

2017 Volume 2, Issue 5, Page(s) 310–319

Abstract: Objective: To provide a review of emerging knowledge from genomics and related basic science, preclinical, and clinical precision medicine studies in head and neck squamous cell carcinoma (HNSCC).: Data sources: The Cancer Genome Atlas Network (TCGA) ...

Abstract	Objective: To provide a review of emerging knowledge from genomics and related basic science, preclinical, and clinical precision medicine studies in head and neck squamous cell carcinoma (HNSCC). Data sources: The Cancer Genome Atlas Network (TCGA) publications, PubMed-based literature review, and ClinicalTrials.gov. Review methods: TCGA publications, PubMed, and ClinicalTrials.gov were queried for genomics and related basic science, preclinical, and developmental clinical precision medicine studies in HNSCC. Results: TCGA reported comprehensive genomic analyses of 279 HNSCC, defining the landscape and frequency of chromosomal copy number alterations, mutations, and expressed genes that contribute to pathogenesis, prognosis, and resistance to therapy. This provides a road map for basic science and preclinical studies to identify key pathways in cancer and cells of the tumor microenvironment affected by these alterations, and candidate targets for new small molecule and biologic therapies. Conclusion: Recurrent chromosomal abnormalities, mutations, and expression of genes affecting HNSCC subsets are associated with differences in prognosis, and define molecules, pathways, and deregulated immune responses as candidates for therapy. Activity of molecularly targeted agents appears to be enhanced by rational combinations of these agents and standard therapies targeting the complex alterations that affect multiple pathways and mechanisms in HNSCC. Level of evidence: NA.
Language	English
Publishing date	2017-08-22
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2378-8038
ISSN	2378-8038
DOI	10.1002/lio2.86
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Article ; Online: Oncogenic Ras and ΔNp63α cooperate to recruit immunosuppressive polymorphonuclear myeloid-derived suppressor cells in a mouse model of squamous cancer pathogenesis.

Sakakibara, Nozomi / Clavijo, Paúl E / Sievers, Cem / Gray, Veronica C / King, Kathryn E / George, Andrea L / Ponnamperuma, Roshini M / Walter, Beatriz A / Chen, Zhong / Van Waes, Carter / Allen, Clint T / Weinberg, Wendy C

Frontiers in immunology

2023 Volume 14, Page(s) 1200970

Abstract: Introduction: Amplification of human chromosome 3q26-29, which encodes oncoprotein ΔNp63 among other isoforms of the p63 family, is a feature common to squamous cell carcinomas (SCCs) of multiple tissue origins. Along with overexpression of ΔNp63, ... ...

Abstract	Introduction: Amplification of human chromosome 3q26-29, which encodes oncoprotein ΔNp63 among other isoforms of the p63 family, is a feature common to squamous cell carcinomas (SCCs) of multiple tissue origins. Along with overexpression of ΔNp63, activation of the protooncogene, Methods: Here, we established and characterized an immune competent mouse model using primary keratinocytes with retroviral-mediated overexpression of ΔNp63α and constitutively activated HRAS (v-ras Results: In this model, orthotopic grafting of wildtype syngeneic keratinocytes expressing both v-ras Conclusion: These results support the utilization of a genetic carcinogenesis model harboring specific genomic drivers of malignancy to study mechanisms underlying the development of local immunosuppression.
MeSH term(s)	Humans ; Animals ; Mice ; Myeloid-Derived Suppressor Cells ; Carcinoma, Squamous Cell/genetics ; Immunosuppressive Agents ; Squamous Cell Carcinoma of Head and Neck ; Disease Models, Animal ; Head and Neck Neoplasms ; Tumor Microenvironment/genetics
Chemical Substances	Immunosuppressive Agents
Language	English
Publishing date	2023-08-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Research Support, N.I.H., Intramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1200970
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Article ; Online: Targeting NF-κB in mouse models of lung adenocarcinoma.

Van Waes, Carter

Cancer discovery

2012 Volume 1, Issue 3, Page(s) 200–202

Abstract: Xue et al. demonstrate response and increased survival but development of acquired resistance to proteasome and inhibitor-κB kinase inhibitors targeting NF-κB activation in adenocarcinomas of Kras-activated, p53-deficient mice. ...

Abstract	Xue et al. demonstrate response and increased survival but development of acquired resistance to proteasome and inhibitor-κB kinase inhibitors targeting NF-κB activation in adenocarcinomas of Kras-activated, p53-deficient mice.
MeSH term(s)	Adenocarcinoma/drug therapy ; Adenocarcinoma of Lung ; Animals ; Antineoplastic Agents/pharmacology ; Lung Neoplasms/drug therapy ; NF-kappa B/antagonists & inhibitors
Chemical Substances	Antineoplastic Agents ; NF-kappa B
Language	English
Publishing date	2012-01-01
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-11-0159
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Article: Combined Inhibition of IAPs and WEE1 Enhances TNFα- and Radiation-Induced Cell Death in Head and Neck Squamous Carcinoma.

Toni, Tiffany / Viswanathan, Ramya / Robbins, Yvette / Gunti, Sreenivasulu / Yang, Xinping / Huynh, Angel / Cheng, Hui / Sowers, Anastasia L / Mitchell, James B / Allen, Clint T / Morgan, Ethan L / Van Waes, Carter

Cancers

2023 Volume 15, Issue 4

Abstract: Head and neck squamous cell carcinoma (HNSCC) remains a prevalent diagnosis with current treatment options that include radiotherapy and immune-mediated therapies, in which tumor necrosis factor-α (TNFα) is a key mediator of cytotoxicity. However, HNSCC ... ...

Abstract	Head and neck squamous cell carcinoma (HNSCC) remains a prevalent diagnosis with current treatment options that include radiotherapy and immune-mediated therapies, in which tumor necrosis factor-α (TNFα) is a key mediator of cytotoxicity. However, HNSCC and other cancers often display TNFα resistance due to activation of the canonical IKK-NFκB/RELA pathway, which is activated by, and induces expression of, cellular inhibitors of apoptosis proteins (cIAPs). Our previous studies have demonstrated that the IAP inhibitor birinapant sensitized HNSCC to TNFα-dependent cell death in vitro and radiotherapy in vivo. Furthermore, we recently demonstrated that the inhibition of the G2/M checkpoint kinase WEE1 also sensitized HNSCC cells to TNFα-dependent cell death, due to the inhibition of the pro-survival IKK-NFκB/RELA complex. Given these observations, we hypothesized that dual-antagonist therapy targeting both IAP and WEE1 proteins may have the potential to synergistically sensitize HNSCC to TNFα-dependent cell death. Using the IAP inhibitor birinapant and the WEE1 inhibitor AZD1775, we show that combination treatment reduced cell viability, proliferation and survival when compared with individual treatment. Furthermore, combination treatment enhanced the sensitivity of HNSCC cells to TNFα-induced cytotoxicity via the induction of apoptosis and DNA damage. Additionally, birinapant and AZD1775 combination treatment decreased cell proliferation and survival in combination with radiotherapy, a critical source of TNFα. These results support further investigation of IAP and WEE1 inhibitor combinations in preclinical and clinical studies in HNSCC.
Language	English
Publishing date	2023-02-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15041029
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Article ; Online: Inhibition of USP14 promotes TNFα-induced cell death in head and neck squamous cell carcinoma (HNSCC).

Morgan, Ethan L / Toni, Tiffany / Viswanathan, Ramya / Robbins, Yvette / Yang, Xinping / Cheng, Hui / Gunti, Sreenivasulu / Huynh, Angel / Sowers, Anastasia L / Mitchell, James B / Allen, Clint T / Chen, Zhong / Van Waes, Carter

Cell death and differentiation

2023 Volume 30, Issue 5, Page(s) 1382–1396

Abstract: TNFα is a key mediator of immune, chemotherapy and radiotherapy-induced cytotoxicity, but several cancers, including head and neck squamous cell carcinomas (HNSCC), display resistance to TNFα due to activation of the canonical NFκB pro-survival pathway. ... ...

Abstract	TNFα is a key mediator of immune, chemotherapy and radiotherapy-induced cytotoxicity, but several cancers, including head and neck squamous cell carcinomas (HNSCC), display resistance to TNFα due to activation of the canonical NFκB pro-survival pathway. However, direct targeting of this pathway is associated with significant toxicity; thus, it is vital to identify novel mechanism(s) contributing to NFκB activation and TNFα resistance in cancer cells. Here, we demonstrate that the expression of proteasome-associated deubiquitinase USP14 is significantly increased in HNSCC and correlates with worse progression free survival in Human Papillomavirus (HPV)- HNSCC. Inhibition or depletion of USP14 inhibited the proliferation and survival of HNSCC cells. Further, USP14 inhibition reduced both basal and TNFα-inducible NFκB activity, NFκB-dependent gene expression and the nuclear translocation of the NFκB subunit RELA. Mechanistically, USP14 bound to both RELA and IκBα and reduced IκBα K48-ubiquitination leading to the degradation of IκBα, a critical inhibitor of the canonical NFκB pathway. Furthermore, we demonstrated that b-AP15, an inhibitor of USP14 and UCHL5, sensitized HNSCC cells to TNFα-mediated cell death, as well as radiation-induced cell death in vitro. Finally, b-AP15 delayed tumor growth and enhanced survival, both as a monotherapy and in combination with radiation, in HNSCC tumor xenograft models in vivo, which could be significantly attenuated by TNFα depletion. These data offer new insights into the activation of NFκB signaling in HNSCC and demonstrate that small molecule inhibitors targeting the ubiquitin pathway warrant further investigation as a novel therapeutic avenue to sensitize these cancers to TNFα- and radiation-induced cytotoxicity.
MeSH term(s)	Humans ; Squamous Cell Carcinoma of Head and Neck/drug therapy ; NF-KappaB Inhibitor alpha/genetics ; Tumor Necrosis Factor-alpha/pharmacology ; Tumor Necrosis Factor-alpha/genetics ; Carcinoma, Squamous Cell/pathology ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/radiotherapy ; NF-kappa B ; Cell Death ; Cell Line, Tumor ; Ubiquitin Thiolesterase/genetics
Chemical Substances	NF-KappaB Inhibitor alpha (139874-52-5) ; Tumor Necrosis Factor-alpha ; NF-kappa B ; USP14 protein, human ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2023-04-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-023-01144-x
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Article ; Online: The Proteomic Landscape of Growth Factor Signaling Networks Associated with

Chen, Zhengjia / Zhang, Chao / Chen, Jianhong / Wang, Dongsheng / Tu, Jieqi / Van Waes, Carter / Saba, Nabil F / Chen, Zhuo G / Chen, Zhong

Cancer research

2021 Volume 81, Issue 17, Page(s) 4402–4416

Abstract: FAT1 is frequently mutated in head and neck squamous cell carcinoma (HNSCC), but the biological and clinical effects ... ...

Abstract	FAT1 is frequently mutated in head and neck squamous cell carcinoma (HNSCC), but the biological and clinical effects of
MeSH term(s)	Cadherins/genetics ; Cadherins/metabolism ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Cluster Analysis ; Databases, Protein ; Disease Progression ; Female ; Gene Expression Profiling ; Genes, Neoplasm ; Genes, erbB-1 ; Genome, Human ; Genomics ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Humans ; Immunologic Factors ; Intercellular Signaling Peptides and Proteins/metabolism ; Kaplan-Meier Estimate ; Male ; Mutation ; Prospective Studies ; Proteomics ; Signal Transduction ; Squamous Cell Carcinoma of Head and Neck/genetics ; Squamous Cell Carcinoma of Head and Neck/metabolism ; Treatment Outcome
Chemical Substances	Cadherins ; FAT1 protein, human ; Immunologic Factors ; Intercellular Signaling Peptides and Proteins
Language	English
Publishing date	2021-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-3659
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Article ; Online: Corrigendum to "The role of protein methyltransferases as potential novel therapeutic targets in squamous cell carcinoma of the head and neck" [Oral Oncol. 81 (2018) 100-108].

Saloura, Vassiliki / Vougiouklakis, Theodore / Burkitt, Kyunghee / Nakamura, Yusuke / Hager, Gordon L / van Waes, Carter

Oral oncology

2018 Volume 86, Page(s) 318

Language	English
Publishing date	2018-09-07
Publishing country	England
Document type	Published Erratum
ZDB-ID	1120465-5
ISSN	1879-0593 ; 0964-1955 ; 1368-8375
ISSN (online)	1879-0593
ISSN	0964-1955 ; 1368-8375
DOI	10.1016/j.oraloncology.2018.08.022
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Zs.A 4869: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Genetic alterations in TRAF3 and CYLD that regulate nuclear factor κB and interferon signaling define head and neck cancer subsets harboring human papillomavirus.

Chen, Tony / Zhang, Jialing / Chen, Zhong / Van Waes, Carter

Cancer

2017 Volume 123, Issue 10, Page(s) 1695–1698

MeSH term(s)	Deubiquitinating Enzyme CYLD ; Head and Neck Neoplasms ; Humans ; Interferons ; NF-kappa B ; Papillomaviridae ; TNF Receptor-Associated Factor 3
Chemical Substances	NF-kappa B ; TNF Receptor-Associated Factor 3 ; TRAF3 protein, human ; Interferons (9008-11-1) ; CYLD protein, human (EC 3.4.19.12) ; Deubiquitinating Enzyme CYLD (EC 3.4.19.12)
Language	English
Publishing date	2017-03-13
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Intramural ; Comment
ZDB-ID	1429-1
ISSN	1097-0142 ; 0008-543X ; 1934-662X
ISSN (online)	1097-0142
ISSN	0008-543X ; 1934-662X
DOI	10.1002/cncr.30659
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Article ; Online: Overcoming barriers to effective immunotherapy: MDSCs, TAMs, and Tregs as mediators of the immunosuppressive microenvironment in head and neck cancer.

Davis, Ruth J / Van Waes, Carter / Allen, Clint T

Oral oncology

2016 Volume 58, Page(s) 59–70

Abstract: A significant subset of head and neck cancers display a T-cell inflamed phenotype, suggesting that patients with these tumors should respond to therapeutic approaches aimed at strengthening anti-tumor immune responses. A major barrier to the development ... ...

Abstract	A significant subset of head and neck cancers display a T-cell inflamed phenotype, suggesting that patients with these tumors should respond to therapeutic approaches aimed at strengthening anti-tumor immune responses. A major barrier to the development of an effective anti-tumor immune response, at baseline or in response to immunotherapy, is the development of an immunosuppressive tumor microenvironment. Several well described mechanisms of effector immune cell suppression in the head and neck cancer microenvironment are discussed here, along with updates on current trials designed to translate what we have learned from pre-clinical and correlative clinical studies into improved responses in patients with head and neck cancer following immune activating therapies.
MeSH term(s)	Head and Neck Neoplasms/immunology ; Humans ; Immune Tolerance ; Immunotherapy ; Macrophages/immunology ; Myeloid-Derived Suppressor Cells/immunology ; T-Lymphocytes, Regulatory/immunology ; Tumor Microenvironment
Language	English
Publishing date	2016-05-20
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1120465-5
ISSN	1879-0593 ; 0964-1955 ; 1368-8375
ISSN (online)	1879-0593
ISSN	0964-1955 ; 1368-8375
DOI	10.1016/j.oraloncology.2016.05.002
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