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      Is Open Access

      Molecularly-targeted therapy for the oral cancer stem cells

      review-article

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Summary

          Human cancer tissues are heterogeneous in nature and become differentiated during expansion of cancer stem cells (CSCs). CSCs initiate tumorigenesis, and are involved in tumor recurrence and metastasis. Furthermore, data show that CSCs are highly resistant to anticancer drugs. Cetuximab, a specific anti-epidermal growth factor receptor (EGFR) monoclonal antibody, is used in cancer treatment. Although development of resistance to cetuximab is well recognized, the underlying mechanisms remain unclear. Lapatinib, a dual inhibitor of epidermal growth factor receptor (EGFR)/ErbB2, has antiproliferative effects and is used to treat patients with ErbB2-positive metastatic breast cancer. In this review, cetuximab and lapatinib-resistant oral squamous cell carcinoma (OSCC) cells proliferation and migration signal transduction passway is discussed by introducing our research.

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          Cellular motility driven by assembly and disassembly of actin filaments.

          Thomas D Pollard, Gary G Borisy (2003)
          Motile cells extend a leading edge by assembling a branched network of actin filaments that produces physical force as the polymers grow beneath the plasma membrane. A core set of proteins including actin, Arp2/3 complex, profilin, capping protein, and ADF/cofilin can reconstitute the process in vitro, and mathematical models of the constituent reactions predict the rate of motion. Signaling pathways converging on WASp/Scar proteins regulate the activity of Arp2/3 complex, which mediates the initiation of new filaments as branches on preexisting filaments. After a brief spurt of growth, capping protein terminates the elongation of the filaments. After filaments have aged by hydrolysis of their bound ATP and dissociation of the gamma phosphate, ADF/cofilin proteins promote debranching and depolymerization. Profilin catalyzes the exchange of ADP for ATP, refilling the pool of ATP-actin monomers bound to profilin, ready for elongation.
          Article 0 comments Cited 571 times – based on 0 reviews     Review now
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            Disruption of epithelial cell-matrix interactions induces apoptosis

            S. Francis, SM Frisch (1994)
            Cell-matrix interactions have major effects upon phenotypic features such as gene regulation, cytoskeletal structure, differentiation, and aspects of cell growth control. Programmed cell death (apoptosis) is crucial for maintaining appropriate cell number and tissue organization. It was therefore of interest to determine whether cell- matrix interactions affect apoptosis. The present report demonstrates that apoptosis was induced by disruption of the interactions between normal epithelial cells and extracellular matrix. We have termed this phenomenon "anoikis." Overexpression of bcl-2 protected cells against anoikis. Cellular sensitivity to anoikis was apparently regulated: (a) anoikis did not occur in normal fibroblasts; (b) it was abrogated in epithelial cells by transformation with v-Ha-ras, v-src, or treatment with phorbol ester; (c) sensitivity to anoikis was conferred upon HT1080 cells or v-Ha-ras-transformed MDCK cells by reverse- transformation with adenovirus E1a; (d) anoikis in MDCK cells was alleviated by the motility factor, scatter factor. The results suggest that the circumvention of anoikis accompanies the acquisition of anchorage independence or cell motility.
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              Fluorouracil, leucovorin, and oxaliplatin with and without cetuximab in the first-line treatment of metastatic colorectal cancer.

              Carsten Bokemeyer, Igor V. Bondarenko, Anatoly Makhson … (2009)
              This randomized study assessed whether the best overall response rate (ORR) of cetuximab combined with oxaliplatin, leucovorin, and fluorouracil (FOLFOX-4) was superior to that of FOLFOX-4 alone as first-line treatment for metastatic colorectal cancer. The influence of KRAS mutation status was investigated. Patients received cetuximab (400 mg/m(2) initial dose followed by 250 mg/m(2)/wk thereafter) plus FOLFOX-4 (oxaliplatin 85 mg/m(2) on day 1, plus leucovorin 200 mg/m(2) and fluorouracil as a 400 mg/m(2) bolus followed by a 600 mg/m(2) infusion during 22 hours on days 1 and 2; n = 169) or FOLFOX-4 alone (n = 168). Treatment was continued until disease progression or unacceptable toxicity. KRAS mutation status was assessed in the subset of patients with assessable tumor samples (n = 233). The confirmed ORR for cetuximab plus FOLFOX-4 was higher than with FOLFOX-4 alone (46% v 36%). A statistically significant increase in the odds for a response with the addition of cetuximab to FOLFOX-4 could not be established (odds ratio = 1.52; P = .064). In patients with KRAS wild-type tumors, the addition of cetuximab to FOLFOX-4 was associated with a clinically significant increased chance of response (ORR = 61% v 37%; odds ratio = 2.54; P = .011) and a lower risk of disease progression (hazard ratio = 0.57; P = .0163) compared with FOLFOX-4 alone. Cetuximab plus FOLFOX-4 was generally well tolerated. KRAS mutational status was shown to be a highly predictive selection criterion in relation to the treatment decision regarding the addition of cetuximab to FOLFOX-4 for previously untreated patients with metastatic colorectal cancer.
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                Author and article information

                Contributors
                Yuichi Ohnishi
                Journal
                Journal ID (nlm-ta): Jpn Dent Sci Rev
                Journal ID (iso-abbrev): Jpn Dent Sci Rev
                Title: The Japanese Dental Science Review
                Publisher: Elsevier
                ISSN (Print): 1882-7616
                ISSN (Electronic): 2213-6851
                Publication date PMC-release: 16 December 2017
                Publication date (Print): May 2018
                Publication date (Electronic): 16 December 2017
                Volume: 54
                Issue: 2
                Pages: 88-103
                Affiliations
                [a ]Second Department of Oral and Maxillofacial Surgery, Osaka Dental University, Hirakata, Osaka 573-1121, Japan
                [b ]Department of Cell Biology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan
                Author notes
                [* ]Corresponding author at: Second Department of Oral and Maxillofacial Surgery, Osaka Dental University, 1-5-17, Otemae, Chuo-ku, Osaka 540-0008, Japan. onishi_yu_ku@ 123456msn.com
                Article
                Publisher ID: S1882-7616(17)30042-X
                DOI: 10.1016/j.jdsr.2017.11.001
                PMC ID: 5944082
                PubMed ID: 29755619
                SO-VID: eff0bb7f-d701-482e-8a72-b64ab03a2a10
                Copyright © © 2017 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 23 May 2017
                Date revision received : 23 October 2017
                Date accepted : 14 November 2017
                Categories
                Subject: Review Article

                Keywords: cancer stem cells,cetuximab,lapatinib,epidermal growth factor receptor,oral squamous cell carcinoma,molecularly-targeted therapy,sphere formation
                Data availability:
                Keywords: cancer stem cells, cetuximab, lapatinib, epidermal growth factor receptor, oral squamous cell carcinoma, molecularly-targeted therapy, sphere formation

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