Special Issue "Cancer Chemoresistance"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 15 October 2018

Special Issue Editor

Guest Editor
Dr. Helen M. Coley

Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK
Website | E-Mail
Phone: +44 (0) 1483 689701
Interests: Drug resistance; Breast cancer; Ovarian cancer; Platinum resistance; New targeted therapies; Epithelial-mesenchymal-transition

Special Issue Information

Dear Colleagues,

In line with numerous other therapeutic agents, the success of cancer drugs is hindered by the development of clinical drug resistance. The scientific community has mounted a considerable effort in order to understand the underlying mechanisms associated with anticancer drug resistance, over a number of decades. These lines of enquiries have resulted in an enrichment of our knowledge of tumour cell biology—but still leave the oncologist with the day-to-day problem of clinical drug resistance.

Identified molecular pathways that can lead to the development of clinical drug resistance include oncogenic drivers, such as EGFR, PI3K/Akt, disrupted DNA repair, cell death pathways, such as apoptosis and autophagy, the presence of ABC transporters and the process of epithelial-mesenchymal-transition (EMT). Much of this work has been supported by developments in bioinformatics, which make use of open-access databases.

In addition to the issues surrounding the use of cytotoxic drugs associated with standard chemotherapy, new targeted agents such as trastuzumab, lapatinib and gefitinib are also known to be associated with the development of gradual clinical drug resistance. Indeed, some of the mechanisms associated with cytotoxic drugs are shared by some of the targeted cancer therapeutic agents. The overall objective for the cancer scientist is to work hand in hand with the oncologist to find ways to predict in advance clinical drug resistance by the use of biomarker development and also to develop strategies to overcome overt drug resistance for example by the use of combination therapies.

Dr. Helen M. Coley
Guest Editor

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 papers will be 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 short 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 monthly 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 1000 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.

Published Papers (2 papers)

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Research

Open AccessArticle miR-1246 Targets CCNG2 to Enhance Cancer Stemness and Chemoresistance in Oral Carcinomas
Cancers 2018, 10(8), 272; https://doi.org/10.3390/cancers10080272
Received: 13 July 2018 / Revised: 7 August 2018 / Accepted: 13 August 2018 / Published: 16 August 2018
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Abstract
MiRNAs have been recognized as crucial components in carcinogenesis, but whether miR-1246 affects the cancer stemness and drug resistance in oral squamous cell carcinoma (OSCC) has not been fully understood and its downstream targets still need to be unraveled. In the present work,
[...] Read more.
MiRNAs have been recognized as crucial components in carcinogenesis, but whether miR-1246 affects the cancer stemness and drug resistance in oral squamous cell carcinoma (OSCC) has not been fully understood and its downstream targets still need to be unraveled. In the present work, we employed miRNAs RT-PCR analysis to evaluate the expression of miR-1246 in tumor tissues and oral cancer stem cells (OCSC). Stemness phenotypes, including self-renewal, migration, invasion, colony formation capacities, and in vivo oncogenicity of oral cancer cells following transfected with miR-1246 inhibitors or mimics were examined. Our results suggested that the expression level of miR-1246 was significantly upregulated in the tumor tissues and OCSC. Kaplan-Meier survival analysis of OSCC patients with high levels of miR-1246 had the worst survival rate compared to their low-expression counterparts. Inhibition of miR-1246 in OCSC significantly reduced the stemness hallmarks, while overexpression of miR-1246 enhanced these characteristics. Moreover, we showed that downregulation of miR-1246 decreased chemoresistance. In addition, we verified that miR-1246-inhibited CCNG2 contributed to the cancer stemness of OSCC. These results demonstrated the significance of miR-1246 in the regulation of OSCC stemness. Targeting miR-1246-CCNG2 axis may be beneficial to suppress cancer relapse and metastasis in OSCC patients. Full article
(This article belongs to the Special Issue Cancer Chemoresistance)
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Open AccessArticle TGF-βRII Knock-down in Pancreatic Cancer Cells Promotes Tumor Growth and Gemcitabine Resistance. Importance of STAT3 Phosphorylation on S727
Cancers 2018, 10(8), 254; https://doi.org/10.3390/cancers10080254
Received: 10 July 2018 / Revised: 26 July 2018 / Accepted: 27 July 2018 / Published: 31 July 2018
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Abstract
Pancreatic adenocarcinoma (PDAC) is one of the most deadly cancers in the Western world because of a lack of early diagnostic markers and efficient therapeutics. At the time of diagnosis, more than 80% of patients have metastasis or locally advanced cancer and are
[...] Read more.
Pancreatic adenocarcinoma (PDAC) is one of the most deadly cancers in the Western world because of a lack of early diagnostic markers and efficient therapeutics. At the time of diagnosis, more than 80% of patients have metastasis or locally advanced cancer and are therefore not eligible for surgical resection. Pancreatic cancer cells also harbour a high resistance to chemotherapeutic drugs such as gemcitabine that is one of the main palliative treatments for PDAC. Proteins involved in TGF-β signaling pathway (SMAD4 or TGF-βRII) are frequently mutated in PDAC (50–80%). TGF-β signalling pathway plays antagonistic roles during carcinogenesis by initially inhibiting epithelial growth and later promoting the progression of advanced tumors and thus emerged as both tumor suppressor and oncogenic pathways. In order to decipher the role of TGF-β in pancreatic carcinogenesis and chemoresistance, we generated CAPAN-1 and CAPAN-2 cell lines knocked down for TGF-βRII (first actor of TGF-β signaling). The impact on biological properties of these TGF-βRII-KD cells was studied both in vitro and in vivo. We show that TGF-βRII silencing alters tumor growth and migration as well as resistance to gemcitabine. TGF-βRII silencing also leads to S727 STAT3 and S63 c-Jun phosphorylation, decrease of MRP3 and increase of MRP4 ABC transporter expression and induction of a partial EMT phenotype. These markers associated with TGF-β signaling pathways may thus appear as potent therapeutic tools to better treat/manage pancreatic cancer. Full article
(This article belongs to the Special Issue Cancer Chemoresistance)
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