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Cancers
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Mechanisms of Cancer Cell Death: Therapeutic Implications
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Mechanisms of Cancer Cell Death: Therapeutic Implications

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 14550

Special Issue Editor

Prof. Dr. Ferenc Gallyas Jr

E-Mail Website
Guest Editor
Department of Biochemistry and Medical Chemistry, University of Pecs Medical School, 7624 Pecs, Hungary
Interests: Non-Hodgkin lymphoma; leukemia; pediatrics; genetics; molecular biology immunology

Special Issue Information

Dear Colleagues,

Cancer is characterized by non-regulated cell division with the potential of invading tissues and organs for the patient apart from the primary site of incidence. Accordingly, most therapeutic approaches aim to kill the cancer cells while harming the normal cells and tissues as little as possible. These efforts are limited to a large extent by innate or acquired resistance of the cancer cells against therapy necessitating the development of novel strategies. Our understanding about the processes leading to the death of cancer cells expanded considerably in the past decades resulting in a number of conceptually new therapeutic means. This Special Issue will provide an up-to-date comprehensive view of the field and stimulate future development. To this end, we welcome original research and review papers on the molecular mechanisms of necrosis, apoptosis, necroptosis, autophagy, pyroptosis, immunogenic cell death, synthetic lethality, and radiation- and chemotherapy-induced cancer cell death. Submissions on novel chemical agents and therapeutic targets are also considered if they likely appeal to general interest.

Dr. Ferenc Gallyas Jr
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 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. Cancers 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 2900 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

  • mitochondria
  • oxidative glycolysis
  • damage-associated molecular patterns
  • tumour microenvironment
  • mitophagy
  • reactive oxygen species
  • natural substances
  • mutation
  • epigenetic alteration
  • cancer stem cells

Published Papers (4 papers)

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Research

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17 pages, 13554 KiB  
Article
A Nuclear-Directed Ribonuclease Variant Targets Cancer Stem Cells and Inhibits Migration and Invasion of Breast Cancer Cells
by Jessica Castro, Giusy Tornillo, Gerardo Ceada, Beatriz Ramos-Neble, Marlon Bravo, Marc Ribó, Maria Vilanova, Matthew J. Smalley and Antoni Benito
Cancers 2021, 13(17), 4350; https://doi.org/10.3390/cancers13174350 - 27 Aug 2021
Cited by 2 | Viewed by 2775
Abstract
Despite the significant advances in cancer research made in recent years, this disease remains one of the leading causes of death worldwide. In part, this is due to the fact that after therapy, a subpopulation of self-renewing tumor cells can survive and promote [...] Read more.
Despite the significant advances in cancer research made in recent years, this disease remains one of the leading causes of death worldwide. In part, this is due to the fact that after therapy, a subpopulation of self-renewing tumor cells can survive and promote cancer relapse, resistance to therapies and metastasis. Targeting these cancer stem cells (CSCs) is therefore essential to improve the clinical outcome of cancer patients. In this sense, multi-targeted drugs may be promising agents targeting CSC-associated multifocal effects. We have previously constructed different human pancreatic ribonuclease (RNase) variants that are cytotoxic for tumor cells due to a non-classical nuclear localization signal introduced in their sequence. These cytotoxic RNases affect the expression of multiple genes involved in deregulated metabolic and signaling pathways in cancer cells and are highly cytotoxic for multidrug-resistant tumor cell lines. Here, we show that these cytotoxic nuclear-directed RNases are highly selective for tumor cell lines grown in 3D, inhibit CSCs’ development and diminish the self-renewal capacity of the CSCs population. Moreover, these human RNase variants reduce the migration and invasiveness of highly invasive breast cancer cells and downregulate N-cadherin expression. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Death: Therapeutic Implications)
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48 pages, 12939 KiB  
Article
Interaction of Adenosine, Modified Using Carborane Clusters, with Ovarian Cancer Cells: A New Anticancer Approach against Chemoresistance
by Katarzyna Bednarska-Szczepaniak, Ewelina Przelazły, Katarzyna Dominika Kania, Marzena Szwed, Miroslava Litecká, Bohumír Grűner and Zbigniew J. Leśnikowski
Cancers 2021, 13(15), 3855; https://doi.org/10.3390/cancers13153855 - 30 Jul 2021
Cited by 13 | Viewed by 3515
Abstract
Platinum compounds remain the first-line drugs for the treatment of most lethal gynecological malignancies and ovarian cancers. Acquired platinum resistance remains a major challenge in gynecological oncology. Considering the unique physicochemical properties of the metallacarboranes modifier and the significant role of nucleoside derivatives [...] Read more.
Platinum compounds remain the first-line drugs for the treatment of most lethal gynecological malignancies and ovarian cancers. Acquired platinum resistance remains a major challenge in gynecological oncology. Considering the unique physicochemical properties of the metallacarboranes modifier and the significant role of nucleoside derivatives as anticancer antimetabolites, we designed and synthesized a set of adenosine conjugates with metallacarboranes containing iron, cobalt, or chromium as semi-abiotic compounds that influence the cisplatin sensitivity of ovarian cancer cells. Adherent cultures of ovarian carcinoma cell lines and multicellular spheroids, ranging from sensitive to highly resistant including experimental cell lines “not responding” to platinum drugs were used. Iron-containing metallacarborane conjugates showed the best anticancer activity, especially against resistant cells. Compound modified at the C2′ nucleoside position showed the best activity in resistant cancer cells and highly resistant cancer spheroids exposed to cisplatin, increasing cell cycle arrest, apoptosis or necrosis, and reactive oxygen species production. Moreover, it showed high cellular accumulation and did not induce cross-resistance to cisplatin, carboplatin, doxorubicin, paclitaxel, or gemcitabine in long-term cultures. The reference nido-carborane derivative (no metal ions) and unmodified nucleosides were not as effective. These findings indicate that metallacarborane modification of adenosine may sensitize ovarian cancer cells to cisplatin in combination treatment. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Death: Therapeutic Implications)
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Review

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15 pages, 1435 KiB  
Review
Emerging Canonical and Non-Canonical Roles of Granzyme B in Health and Disease
by Ellis Tibbs and Xuefang Cao
Cancers 2022, 14(6), 1436; https://doi.org/10.3390/cancers14061436 - 10 Mar 2022
Cited by 17 | Viewed by 4275
Abstract
The Granzyme (Gzm) family has classically been recognized as a cytotoxic tool utilized by cytotoxic T lymphocytes (CTL) and natural killer (NK) cells to illicit cell death to infected and cancerous cells. Their importance is established based on evidence showing that deficiencies in [...] Read more.
The Granzyme (Gzm) family has classically been recognized as a cytotoxic tool utilized by cytotoxic T lymphocytes (CTL) and natural killer (NK) cells to illicit cell death to infected and cancerous cells. Their importance is established based on evidence showing that deficiencies in these cell death executors result in defective immune responses. Recent findings have shown the importance of Granzyme B (GzmB) in regulatory immune cells, which may contribute to tumor growth and immune evasion during cancer development. Other studies have shown that members of the Gzm family are important for biological processes such as extracellular matrix remodeling, angiogenesis and organized vascular degradation. With this growing body of evidence, it is becoming more important to understand the broader function of Gzm’s rather than a specific executor of cell death, and we should be aware of the many alternative roles that Gzm’s play in physiological and pathological conditions. Therefore, we review the classical as well as novel non-canonical functions of GzmB and discuss approaches to utilize these new findings to address current gaps in our understanding of the immune system and tissue development. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Death: Therapeutic Implications)
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19 pages, 2011 KiB  
Review
Mechanisms of Cancer Cell Death: Therapeutic Implications for Pancreatic Ductal Adenocarcinoma
by Hannah Pook and Siim Pauklin
Cancers 2021, 13(19), 4834; https://doi.org/10.3390/cancers13194834 - 28 Sep 2021
Cited by 5 | Viewed by 2904
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a type of cancer that is strongly associated with poor prognosis and short median survival times. In stark contrast to the progress seen in other cancer types in recent decades, discoveries of new treatments in PDAC have been [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is a type of cancer that is strongly associated with poor prognosis and short median survival times. In stark contrast to the progress seen in other cancer types in recent decades, discoveries of new treatments in PDAC have been few and far between and there has been little improvement in overall survival (OS). The difficulty in treating this disease is multifactorial, contributed to by late presentation, difficult access to primary tumour sites, an ‘immunologically cold’ phenotype, and a strong tendency of recurrence likely driven by cancer stem cell (CSC) populations. Furthermore, apparently contrasting roles of tumour components (such as fibrotic stroma) and intracellular pathways (such as autophagy and TGFβ) have made it difficult to distinguish beneficial from detrimental drug targets. Despite this, progress has been made in the field, including the determination of mFOLFIRINOX as the standard-of-care adjuvant therapy and the discovery of KRASG12C mutant inhibitors. Moreover, new research, as outlined in this review, has highlighted promising new approaches including the targeting of the tumour microenvironment, enhancement of immunotherapies, epigenetic modulation, and destruction of CSCs. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Death: Therapeutic Implications)
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