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Cancers
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Apoptosis in Cancer 2.0
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Apoptosis in Cancer 2.0

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

Deadline for manuscript submissions: 30 November 2024 | Viewed by 5703

Special Issue Editor

Prof. Dr. Arun Dharmarajan

E-Mail Website1 Website2
Guest Editor
1. School of Pharmacy and Biomedical Sciences, Curtin Health Innovation Research Institute (CHIRI), Curtin University, Perth, WA, Australia
2. Department of Biomedical Sciences, Faculty of Biomedical Sciences, Technology and Research, Sriramachandra Institute of Higher Education and Research, Chennai, India
3. School of Human Sciences, The University of Western Australia, Nedlands, Perth, WA 6009, Australia
Interests: Wnt signaling; secreted frizzled related protein 4; cancer; cancer stem cells; angiogenesis; apoptosis; redox signaling; molecular modeling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This collection is the second edition of a previous Special Issue titled “Apoptosis in Cancer” (https://www.mdpi.com/journal/cancers/special_issues/Apoptosis_cancer). 

In the last decade, basic cancer research has produced remarkable advances in our understanding of cancer biology and cancer genetics. Among the most important of these advances is the realization that apoptosis and the genes that control it have a profound effect on the malignant phenotype. For example, it is now clear that some oncogenic mutations disrupt the apoptotic process, leading to tumor initiation, progression, and finally metastasis. It is also well documented that most cytotoxic anticancer agents induce apoptosis, raising the intriguing possibility that deregulation in apoptotic programs contributes to treatment failure. Apoptosis is mechanistically governed through two main pathways: the extrinsic (death receptor-mediated) and the intrinsic, or the mitochondrial pathway, which is activated in response to cellular damage induced through radiation, hypoxia, and some anticancer agents. Dysregulation of these apoptotic pathways can result in the resistance of cell death and is a hallmark of cancer. Consequently, targeting key regulatory proteins within these pathways has been a primary focus of many cancer studies. A prototypical example of this is the targeting of B-cell lymphoma 2 (BCL-2) family of proteins. The primary focus of this topic will be cell signaling in apoptosis, mitochondrial-mediated apoptosis, and novel compounds to target apoptosis and cancer. In addition, reviews and research articles will explore the mechanisms of apoptosis and the ways in which tumor cells modulate these processes to induce their survival and examine current clinical modalities aimed at exploiting these defects to selectively induce apoptosis in tumor cells.

Prof. Dr. Arun Dharmarajan
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

  • apoptosis
  • cancer
  • redox signaling
  • Wnt
  • oncogenes
  • frizzled

Published Papers (3 papers)

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Research

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16 pages, 2618 KiB  
Article
Methanodibenzo[b,f][1,5]dioxocins as Novel Glutaminase Inhibitor with Anti-Glioblastoma Potential
by Akshaya Murugesan, Sana Kari, Anita Shrestha, Benedicta Assoah, Konda Mani Saravanan, Monica Murugesan, Ramesh Thiyagarajan, Nuno R. Candeias and Meenakshisundaram Kandhavelu
Cancers 2023, 15(4), 1010; https://doi.org/10.3390/cancers15041010 - 5 Feb 2023
Viewed by 1681
Abstract
Glutamine metabolism is an important hallmark of several cancers with demonstrated antitumor activity in glioblastoma cancer cells (GBM). GBM cells regulate glutamine and use it as a major energy source for their proliferation through the glutaminolysis process. Enzymes, such as glutaminase in glutaminolysis, [...] Read more.
Glutamine metabolism is an important hallmark of several cancers with demonstrated antitumor activity in glioblastoma cancer cells (GBM). GBM cells regulate glutamine and use it as a major energy source for their proliferation through the glutaminolysis process. Enzymes, such as glutaminase in glutaminolysis, can be targeted by small-molecule inhibitors, thus exhibiting promising anticancer properties. The resistance to glutaminolysis demands the development of new therapeutic molecules to overcome drug resistance. Herein, we have reported a novel library of constrained methanodibenzo[b,f][1,5]dioxocin derivatives as glutaminase (GLS) inhibitors and their anti-GBM potential. The library consisting of seven molecules was obtained through self-condensation of 2′-hydroxyacetophenones, out of which three molecules, namely compounds 3, 5, and 6, were identified with higher binding energy values ranging between −10.2 and −9.8 kcal/mol with GLS (PDB ID; 4O7D). Pharmacological validation of these compounds also showed a higher growth inhibition effect in GBM cells than the standard drug temozolomide (TMZ). The most promising compound, 6, obeyed Lipinski’s rule of five and was identified to interact with key residues Arg307, Asp326, Lys328, Lys399, and Glu403 of GLS. This compound exhibited the best cytotoxic effect with IC50 values of 63 µM and 83 µM in LN229 and SNB19 cells, respectively. The potential activation of GLS by the best-constrained dibenzo[b,f][1,5]dioxocin in the tested series increased apoptosis via reactive oxygen species production in both GBM cells, and exhibited anti-migratory and anti-proliferative properties over time in both cell lines. Our results highlight the activation mechanism of a dibenzo[b,f][1,5]dioxocin from the structural basis and demonstrate that inhibition of glutaminolysis may facilitate the pharmacological intervention for GBM treatment. Full article
(This article belongs to the Special Issue Apoptosis in Cancer 2.0)
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Review

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13 pages, 2288 KiB  
Review
Interleukin 24: Signal Transduction Pathways
by Simira Smith, Sual Lopez, Anastassiya Kim, Justina Kasteri, Ezekiel Olumuyide, Kristian Punu, Columba de la Parra and Moira Sauane
Cancers 2023, 15(13), 3365; https://doi.org/10.3390/cancers15133365 - 27 Jun 2023
Cited by 1 | Viewed by 1853
Abstract
Interleukin 24 is a member of the IL-10 family with crucial roles in antitumor, wound healing responses, host defense, immune regulation, and inflammation. Interleukin 24 is produced by both immune and nonimmune cells. Its canonical pathway relies on recognition and interaction with specific [...] Read more.
Interleukin 24 is a member of the IL-10 family with crucial roles in antitumor, wound healing responses, host defense, immune regulation, and inflammation. Interleukin 24 is produced by both immune and nonimmune cells. Its canonical pathway relies on recognition and interaction with specific Interleukin 20 receptors in the plasma membrane and subsequent cytoplasmic Janus protein tyrosine kinases (JAK)/signal transducer and activator of the transcription (STAT) activation. The identification of noncanonical JAK/STAT-independent signaling pathways downstream of IL-24 relies on the interaction of IL-24 with protein kinase R in the cytosol, respiratory chain proteins in the inner mitochondrial membrane, and chaperones such as Sigma 1 Receptor in the endoplasmic reticulum. Numerous studies have shown that enhancing or inhibiting the expression of Interleukin 24 has a therapeutic effect in animal models and clinical trials in different pathologies. Successful drug targeting will require a deeper understanding of the downstream signaling pathways. In this review, we discuss the signaling pathway triggered by IL-24. Full article
(This article belongs to the Special Issue Apoptosis in Cancer 2.0)
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15 pages, 1049 KiB  
Review
The Sweet Side of HIPK2
by Alessia Garufi, Valerio D’Orazi, Giuseppa Pistritto, Mara Cirone and Gabriella D’Orazi
Cancers 2023, 15(10), 2678; https://doi.org/10.3390/cancers15102678 - 9 May 2023
Cited by 2 | Viewed by 1718
Abstract
HIPK2 is an evolutionary conserved protein kinase which modulates many molecular pathways involved in cellular functions such as apoptosis, DNA damage response, protein stability, and protein transcription. HIPK2 plays a key role in the cancer cell response to cytotoxic drugs as its deregulation [...] Read more.
HIPK2 is an evolutionary conserved protein kinase which modulates many molecular pathways involved in cellular functions such as apoptosis, DNA damage response, protein stability, and protein transcription. HIPK2 plays a key role in the cancer cell response to cytotoxic drugs as its deregulation impairs drug-induced cancer cell death. HIPK2 has also been involved in regulating fibrosis, angiogenesis, and neurological diseases. Recently, hyperglycemia was found to positively and/or negatively regulate HIPK2 activity, affecting not only cancer cell response to chemotherapy but also the progression of some diabetes complications. The present review will discuss how HIPK2 may be influenced by the high glucose (HG) metabolic condition and the consequences of such regulation in medical conditions. Full article
(This article belongs to the Special Issue Apoptosis in Cancer 2.0)
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