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      Targeting cancer stem cells in squamous cell carcinoma

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          Abstract

          Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive tumor and the sixth most common cancer worldwide. Current treatment strategies for HNSCC are surgery, radiotherapy, chemotherapy, immunotherapy or combinatorial therapies. However, the overall 5-year survival rate of HNSCC patients remains at about 50%. Cancer stem cells (CSCs), a small population among tumor cells, are able to self-renew and differentiate into different tumor cell types in a hierarchical manner, similar to normal tissue. In HNSCC, CSCs are proposed to be responsible for tumor initiation, progression, metastasis, drug resistance, and recurrence. In this review, we discuss the molecular and cellular characteristics of CSCs in HNSCC. We summarize current approaches used in the literature for identification of HNSCC CSCs, and mechanisms required for CSC regulation. We also highlight the role of CSCs in treatment failure and therapeutic targeting options for eliminating CSCs in HNSCC.

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          Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1.

          N. Agrawal, M Frederick, C. R. Pickering … (2011)
          Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. To explore the genetic origins of this cancer, we used whole-exome sequencing and gene copy number analyses to study 32 primary tumors. Tumors from patients with a history of tobacco use had more mutations than did tumors from patients who did not use tobacco, and tumors that were negative for human papillomavirus (HPV) had more mutations than did HPV-positive tumors. Six of the genes that were mutated in multiple tumors were assessed in up to 88 additional HNSCCs. In addition to previously described mutations in TP53, CDKN2A, PIK3CA, and HRAS, we identified mutations in FBXW7 and NOTCH1. Nearly 40% of the 28 mutations identified in NOTCH1 were predicted to truncate the gene product, suggesting that NOTCH1 may function as a tumor suppressor gene rather than an oncogene in this tumor type.
          Article 0 comments Cited 612 times – based on 0 reviews     Review now
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            Role of histone H2A ubiquitination in Polycomb silencing.

            Hengbin Wang, Liangjun Wang, Hediye Erdjument-Bromage … (2004)
            Covalent modification of histones is important in regulating chromatin dynamics and transcription. One example of such modification is ubiquitination, which mainly occurs on histones H2A and H2B. Although recent studies have uncovered the enzymes involved in histone H2B ubiquitination and a 'cross-talk' between H2B ubiquitination and histone methylation, the responsible enzymes and the functions of H2A ubiquitination are unknown. Here we report the purification and functional characterization of an E3 ubiquitin ligase complex that is specific for histone H2A. The complex, termed hPRC1L (human Polycomb repressive complex 1-like), is composed of several Polycomb-group proteins including Ring1, Ring2, Bmi1 and HPH2. hPRC1L monoubiquitinates nucleosomal histone H2A at lysine 119. Reducing the expression of Ring2 results in a dramatic decrease in the level of ubiquitinated H2A in HeLa cells. Chromatin immunoprecipitation analysis demonstrated colocalization of dRing with ubiquitinated H2A at the PRE and promoter regions of the Drosophila Ubx gene in wing imaginal discs. Removal of dRing in SL2 tissue culture cells by RNA interference resulted in loss of H2A ubiquitination concomitant with derepression of Ubx. Thus, our studies identify the H2A ubiquitin ligase, and link H2A ubiquitination to Polycomb silencing.
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              Formation of pluripotent stem cells in the mammalian embryo depends on the POU transcription factor Oct4.

              J. Nichols, B Zevnik, K Anastassiadis … (1998)
              Oct4 is a mammalian POU transcription factor expressed by early embryo cells and germ cells. We report that the activity of Oct4 is essential for the identity of the pluripotential founder cell population in the mammalian embryo. Oct4-deficient embryos develop to the blastocyst stage, but the inner cell mass cells are not pluripotent. Instead, they are restricted to differentiation along the extraembryonic trophoblast lineage. Furthermore, in the absence of a true inner cell mass, trophoblast proliferation is not maintained in Oct4-/- embryos. Expansion of trophoblast precursors is restored, however, by an Oct4 target gene product, fibroblast growth factor-4. Therefore, Oct4 also determines paracrine growth factor signaling from stem cells to the trophectoderm.
              Article 0 comments Cited 454 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Demeng Chen
                Cun-Yu Wang
                Journal
                Journal ID (nlm-ta): Precis Clin Med
                Journal ID (iso-abbrev): Precis Clin Med
                Journal ID (publisher-id): pcm
                Title: Precision Clinical Medicine
                Publisher: Oxford University Press
                ISSN (Print): 2096-5303
                ISSN (Electronic): 2516-1571
                Publication date (Print): September 2019
                Publication date (Electronic): 01 October 2019
                Publication date PMC-release: 01 October 2019
                Volume: 2
                Issue: 3
                Pages: 152-165
                Affiliations
                [1 ] Laboratory of Molecular Signaling , Division of Oral Biology and Medicine, School of Dentistry, UCLA, Los Angeles, CA 90095, USA
                [2 ] Department of Bioengineering , Henry Samueli School of Engineering and Applied Science, UCLA, Los Angeles, CA 90095, USA
                [3 ] Jonsson Comprehensive Cancer Center and Broad Stem Cell Research Center , UCLA, Los Angeles, CA 90095, USA
                Author notes
                Correspondence: Demeng Chen, chendm29@ 123456mail.sysu.edu.cn ; Cun-Yu Wang, cwang@ 123456dentistry.ucla.edu
                Article
                Publisher ID: pbz016
                DOI: 10.1093/pcmedi/pbz016
                PMC ID: 6770277
                PubMed ID: 31598386
                SO-VID: 188a7031-aa56-49e8-bf56-bf379f5fc047
                Copyright © © The Author(s) 2019. Published by Oxford University Press on behalf of West China School of Medicine & West China Hospital of Sichuan University.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 18 June 2019
                Date revision received : 14 August 2019
                Date accepted : 14 August 2019
                Page count
                Pages: 14
                Funding
                Funded by: National Institutes of Health 10.13039/100000002
                Award ID: R01 DE15964
                Categories
                Subject: Review

                Keywords: cancer stem cells,head and neck squamous cell carcinoma,lymph node metastasis,resistance
                Data availability:
                Keywords: cancer stem cells, head and neck squamous cell carcinoma, lymph node metastasis, resistance

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