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Cells
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Innovative Drug Treatment of Cancer Cells
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Innovative Drug Treatment of Cancer Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (20 October 2022) | Viewed by 18223

Special Issue Editors

Dr. Isabelle Mus-Veteau

E-Mail Website
Guest Editor
Institute of Molecular and Cellular Pharmacology (IPMC), French National Centre for Scientific Research (CNRS), 06560 Valbonne, France
Interests: drug efflux; multidrug transporter; resistance to chemotherapy; cancer persistent cells
Dr. Frédéric Luton

E-Mail Website
Guest Editor
Institute of Molecular and Cellular Pharmacology (IPMC), French National Centre for Scientific Research (CNRS), 06560 Valbonne, France
Interests: cancer cells; isolating drugs to control tumour cell invasion; cancer metastasis; breast cancer

Special Issue Information

Dear Colleagues,

Cancer is among the leading causes of death worldwide. Tumor removal by surgery is the most important step in the management of patients with cancers. However, too many patients who undergo surgery have a low survival rate due to the advanced stage of their disease at the moment of diagnosis, which makes the complete removal of the tumor with surgery impossible; thus, they often relapse after resection. Many patients present a high risk of relapse and metastasis even when the primary tumor is diagnosed and surgically excised at an early stage. Chemotherapy is often used to improve the recurrence-free survival of patients. Patients with blood cancer are also often treated with chemotherapy, which sometimes consists of the use of several drugs together in a set regimen. However, a minority of patients experience a sustained benefit of this treatment, which unfortunately presents side effects so severe that it often makes the patients unable to attain target drug doses shown to give a survival benefit. The Special Issue on the "Innovative Drug Treatment of Cancer Cells” will focus on new therapeutic options to improve cancer treatment outcomes and increase the overall survival of patients. We encourage the submission of manuscripts (original research and reviews) highlighting present efforts to study, at the cellular level, innovative compounds targeting cancer cells and cancer stem cells responsible for relapse and metastases, including new drugs targeting already-known targets of cancer cells, drugs targeting new specific targets of cancer cells or cancer stem cells, and new combinations of targeted or classical chemotherapies.

Dr. Isabelle Mus-Veteau
Dr. Frédéric Luton
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 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. Cells 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 2700 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

  • cancer
  • cancer stem cells
  • primary tumor
  • relapse
  • metastases
  • new cancer targets
  • chemotherapy
  • medicinal chemistry
  • pharmacology

Published Papers (7 papers)

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Research

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12 pages, 10084 KiB  
Article
Engineered Synthetic STxB for Enhanced Cytosolic Delivery
by Justine Hadjerci, Anne Billet, Pascal Kessler, Gilles Mourier, Marine Ghazarian, Anthony Gonzalez, Christian Wunder, Nesrine Mabrouk, Eric Tartour, Denis Servent and Ludger Johannes
Cells 2023, 12(9), 1291; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12091291 - 30 Apr 2023
Viewed by 1753
Abstract
Many molecular targets for cancer therapy are located in the cytosol. Therapeutic macromolecules are generally not able to spontaneously translocate across membranes to reach these cytosolic targets. Therefore a strong need exists for tools that enhance cytosolic delivery. Shiga toxin B-subunit (STxB) is [...] Read more.
Many molecular targets for cancer therapy are located in the cytosol. Therapeutic macromolecules are generally not able to spontaneously translocate across membranes to reach these cytosolic targets. Therefore a strong need exists for tools that enhance cytosolic delivery. Shiga toxin B-subunit (STxB) is used to deliver therapeutic principles to disease-relevant cells that express its receptor, the glycolipid Gb3. Based on its naturally existing membrane translocation capacity, STxB delivers antigens to the cytosol of Gb3-positive dendritic cells, leading to the induction of CD8+ T cells. Here, we have explored the possibility of further increasing the membrane translocation of STxB to enable other therapeutic applications. For this, our capacity to synthesize STxB chemically was exploited to introduce unnatural amino acids at different positions of the protein. These were then functionalized with hydrophobic entities to locally destabilize endosomal membranes. Intracellular trafficking of these functionalized STxB was measured by confocal microscopy and their cytosolic arrival with a recently developed highly robust, sensitive, and quantitative translocation assay. From different types of hydrophobic moieties that were linked to STxB, the most efficient configuration was determined. STxB translocation was increased by a factor of 2.5, paving the path for new biomedical opportunities. Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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15 pages, 4213 KiB  
Article
Pharmacodynamic Modeling to Evaluate the Impact of Cimetidine, an OCT2 Inhibitor, on the Anticancer Effects of Cisplatin
by Hardik Mody, Tanaya R. Vaidya, Lawrence J. Lesko and Sihem Ait-Oudhia
Cells 2023, 12(1), 57; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12010057 - 23 Dec 2022
Cited by 1 | Viewed by 1860
Abstract
Despite potent anticancer activity, the clinical utilization of cisplatin is limited due to nephrotoxicity. As Organic Cation Transporter 2 (OCT2) has been shown to be one of the key transporters involved in the uptake of cisplatin into renal proximal tubules, OCT2 inhibitors such [...] Read more.
Despite potent anticancer activity, the clinical utilization of cisplatin is limited due to nephrotoxicity. As Organic Cation Transporter 2 (OCT2) has been shown to be one of the key transporters involved in the uptake of cisplatin into renal proximal tubules, OCT2 inhibitors such as cimetidine have been explored to suppress cisplatin-induced nephrotoxicity. Nonetheless, the impact of OCT2 inhibition or cimetidine on the anti-cancer effects of cisplatin has not been extensively examined. The main objective of the present study was to quantitatively characterize the anticancer effects of cisplatin and cimetidine and determine their nature of interactions in two cancer cell lines, OCT2-negative hepatocellular carcinoma (HCC) cell line, Huh7, and OCT2-positive breast cancer cell line, MDA-MB-468. First, we determined the static concentration-response curves of cisplatin and cimetidine as single agents. Next, with the help of three-dimensional (3D) response surface analyses and a competitive interaction model, we determined their nature of interactions at static concentrations to be modestly synergistic or additive in Huh7 and antagonistic in MDA-MB-468. These results were consistent with the cell-level pharmacodynamic (PD) modeling analysis which leveraged the time-course effects of drugs as single agents and drug combinations. Our developed PD model can be further used to design future preclinical studies to further investigate the cisplatin and cimetidine combinations in different in vitro and in vivo cancer models. Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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13 pages, 1768 KiB  
Article
Search for Synergistic Drug Combinations to Treat Chronic Lymphocytic Leukemia
by Eleonora Ela Hezkiy, Santosh Kumar, Valid Gahramanov, Julia Yaglom, Arkadi Hesin, Suchita Suryakant Jadhav, Ekaterina Guzev, Shivani Patel, Elena Avinery, Michael A. Firer and Michael Y. Sherman
Cells 2022, 11(22), 3671; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11223671 - 18 Nov 2022
Viewed by 1784
Abstract
Finding synergistic drug combinations is an important area of cancer research. Here, we sought to rationally design synergistic drug combinations with an inhibitor of BTK kinase, ibrutinib, which is used for the treatment of several types of leukemia. We (a) used a pooled [...] Read more.
Finding synergistic drug combinations is an important area of cancer research. Here, we sought to rationally design synergistic drug combinations with an inhibitor of BTK kinase, ibrutinib, which is used for the treatment of several types of leukemia. We (a) used a pooled shRNA screen to identify genes that protect cells from the drug, (b) identified protective pathways via bioinformatics analysis of these gene sets, and (c) identified drugs that inhibit these pathways. Based on this analysis, we established that inhibitors of proteasome and mTORC1 could synergize with ibrutinib both in vitro and in vivo. We suggest that FDA-approved inhibitors of these pathways could be effectively combined with ibrutinib for the treatment of chronic lymphocytic leukemia (CLL). Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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20 pages, 4566 KiB  
Article
Regorafenib Induces Senescence and Epithelial-Mesenchymal Transition in Colorectal Cancer to Promote Drug Resistance
by Pashalina Kehagias, Nadège Kindt, Mohammad Krayem, Ahmad Najem, Giulia Agostini, Elena Acedo Reina, Giacomo Bregni, Francesco Sclafani, Fabrice Journe, Ahmad Awada, Ghanem E. Ghanem and Alain Hendlisz
Cells 2022, 11(22), 3663; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11223663 - 18 Nov 2022
Cited by 6 | Viewed by 2227
Abstract
Potential intrinsic resistance mechanisms to regorafenib were explored after short exposure (3 days) on five CRC cell lines (HCT-116, SW1116, LS-1034, SW480, Caco-2). The observation of senescence-like features led to the investigation of a drug-initiated phenotype switch. Following long-term exposure (12 months) of [...] Read more.
Potential intrinsic resistance mechanisms to regorafenib were explored after short exposure (3 days) on five CRC cell lines (HCT-116, SW1116, LS-1034, SW480, Caco-2). The observation of senescence-like features led to the investigation of a drug-initiated phenotype switch. Following long-term exposure (12 months) of HCT-116 and SW480 cell lines to regorafenib, we developed resistant models to explore acquired resistance. SW480 cells demonstrated senescent-like properties, including a cell arrest in the late G2/prophase cell cycle stage and a statistically significant decrease in the expression of G1 Cyclin-Dependent Kinase inhibitors and key cell cycle regulators. A specific senescence-associated secretome was also observed. In contrast, HCT-116 treated cells presented early senescent features and developed acquired resistance triggering EMT and a more aggressive phenotype over time. The gained migration and invasion ability by long-exposed cells was associated with the increased expression level of key cellular and extracellular EMT-related factors. The PI3K/AKT pathway was a significant player in the acquired resistance of HCT-116 cells, possibly related to a PI3KCA mutation in this cell line. Our findings provide new insights into the phenotypic plasticity of CRC cells able, under treatment pressure, to acquire a stable TIS or to use an early senescence state to undergo EMT. Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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15 pages, 3643 KiB  
Article
Inhibition of DNA Repair by Inappropriate Activation of ATM, PARP, and DNA-PK with the Drug Agonist AsiDNA
by Nathalie Berthault, Ptissam Bergam, Floriane Pereira, Pierre-Marie Girard and Marie Dutreix
Cells 2022, 11(14), 2149; https://doi.org/10.3390/cells11142149 - 8 Jul 2022
Cited by 2 | Viewed by 1883
Abstract
AsiDNA is a DNA repair inhibitor mimicking DNA double-strand breaks (DSB) that was designed to disorganize DSB repair pathways to sensitize tumors to DNA damaging therapies such as radiotherapy and chemotherapy. We used the property of AsiDNA of triggering artificial DNA damage signaling [...] Read more.
AsiDNA is a DNA repair inhibitor mimicking DNA double-strand breaks (DSB) that was designed to disorganize DSB repair pathways to sensitize tumors to DNA damaging therapies such as radiotherapy and chemotherapy. We used the property of AsiDNA of triggering artificial DNA damage signaling to examine the activation of DSB repair pathways and to study the main steps of inhibition of DNA repair foci after irradiation. We show that, upon AsiDNA cellular uptake, cytoplasmic ATM and PARP are rapidly activated (within one hour) even in the absence of irradiation. ATM activation by AsiDNA leads to its transient autophosphorylation and sequestration in the cytoplasm, preventing the formation of ATM nuclear foci on irradiation-induced damage. In contrast, the activation of PARP did not seem to alter its ability to form DNA repair foci, but prevented 53BP1 and XRCC4 recruitment at the damage sites. In the nucleus, AsiDNA is essentially associated with DNA-PK, which triggers its activation leading to phosphorylation of H2AX all over chromatin. This pan-nuclear phosphorylation of H2AX correlates with the massive inhibition, at damage sites induced by irradiation, of the recruitment of repair enzymes involved in DSB repair by homologous recombination and nonhomologous end joining. These results highlight the interest in a new generation of DNA repair inhibitors targeting DNA damage signaling. Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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Review

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20 pages, 1173 KiB  
Review
RHOA Therapeutic Targeting in Hematological Cancers
by Juliana Carvalho Santos, Núria Profitós-Pelejà, Salvador Sánchez-Vinces and Gaël Roué
Cells 2023, 12(3), 433; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12030433 - 28 Jan 2023
Cited by 6 | Viewed by 2825
Abstract
Primarily identified as an important regulator of cytoskeletal dynamics, the small GTPase Ras homolog gene family member A (RHOA) has been implicated in the transduction of signals regulating a broad range of cellular functions such as cell survival, migration, adhesion and proliferation. Deregulated [...] Read more.
Primarily identified as an important regulator of cytoskeletal dynamics, the small GTPase Ras homolog gene family member A (RHOA) has been implicated in the transduction of signals regulating a broad range of cellular functions such as cell survival, migration, adhesion and proliferation. Deregulated activity of RHOA has been linked to the growth, progression and metastasis of various cancer types. Recent cancer genome-wide sequencing studies have unveiled both RHOA gain and loss-of-function mutations in primary leukemia/lymphoma, suggesting that this GTPase may exert tumor-promoting or tumor-suppressive functions depending on the cellular context. Based on these observations, RHOA signaling represents an attractive therapeutic target for the development of selective anticancer strategies. In this review, we will summarize the molecular mechanisms underlying RHOA GTPase functions in immune regulation and in the development of hematological neoplasms and will discuss the current strategies aimed at modulating RHOA functions in these diseases. Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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24 pages, 1869 KiB  
Review
Biomarker-Targeted Therapies in Non–Small Cell Lung Cancer: Current Status and Perspectives
by Haiyang Guo, Jun Zhang, Chao Qin, Hang Yan, Tao Liu, Haiyang Hu, Shengjie Tang, Shoujun Tang and Haining Zhou
Cells 2022, 11(20), 3200; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11203200 - 12 Oct 2022
Cited by 19 | Viewed by 4898
Abstract
Non-small-cell lung cancer (NSCLC) is one of the most common malignancies and the leading causes of cancer-related death worldwide. Despite many therapeutic advances in the past decade, NSCLC remains an incurable disease for the majority of patients. Molecular targeted therapies and immunotherapies have [...] Read more.
Non-small-cell lung cancer (NSCLC) is one of the most common malignancies and the leading causes of cancer-related death worldwide. Despite many therapeutic advances in the past decade, NSCLC remains an incurable disease for the majority of patients. Molecular targeted therapies and immunotherapies have significantly improved the prognosis of NSCLC. However, the vast majority of advanced NSCLC develop resistance to current therapies and eventually progress. In this review, we discuss current and potential therapies for NSCLC, focusing on targeted therapies and immunotherapies. We highlight the future role of metabolic therapies and combination therapies in NSCLC. Full article
(This article belongs to the Special Issue Innovative Drug Treatment of Cancer Cells)
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