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Cancers
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The Role of Autophagy in Brain Tumors
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The Role of Autophagy in Brain Tumors

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

Deadline for manuscript submissions: closed (1 May 2023) | Viewed by 14058

Special Issue Editor

Dr. Gabriella D’Orazi

E-Mail Website
Guest Editor
1. Department of Neuroscience and Imaging, University G. D’Annunzio, 66013 Chieti, Italy
2. Department of Research, Unit of Cellular Network and Therapeutic Innovation, Regina Elena National Cancer Institute, 00144 Rome, Italy
Interests: tumor biology; molecular oncology; onco-suppressor p53; autophagy; hypoxia; oxidative stress; tumor microenvironment; glioblastoma; personalized medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain tumors include a broad range of primary and metastatic tumors and are among the most threatening diseases worldwide. Surgical interventions, although improved in recent years, cannot often completely eradicate brain tumors that rather progress and metastasize, reducing the patient survival. The current therapeutic options, such as radio- and chemo-therapies, and immunotherapy, are also not so effective because brain tumors are highly resistant to therapies. Autophagy is a highly conserved cellular homeostatic process; however, its deregulation is associated with several pathological processes including cancer. Therefore, autophagy manipulation could be exploited to improve the outcome of cancer treatment.

This Special Issue will focus on autophagy manipulation in brain tumors for therapeutic purpose. We are pleased to invite authors to submit contributions, such as original articles that provide novel findings, or reviews that comprehensively highlight the latest discoveries in the field.

I look forward to receiving your contribution.

Dr. Gabriella D'Orazi
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 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

  • glioblastomas
  • cancer treatment
  • chemoresistance
  • autophagy
  • autophagy inhibitors
  • autophagy activators
  • novel therapeutics
  • targeted therapy
  • personalized therapy

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Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 190 KiB  
Editorial
The Role of Autophagy in Brain Tumors
by Gabriella D’Orazi
Cancers 2023, 15(19), 4802; https://doi.org/10.3390/cancers15194802 - 29 Sep 2023
Viewed by 833
Abstract
Primary and metastatic brain tumors are among the most threatening diseases worldwide [...] Full article
(This article belongs to the Special Issue The Role of Autophagy in Brain Tumors)

Research

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21 pages, 6470 KiB  
Article
Sodium Propionate Contributes to Tumor Cell Growth Inhibition through PPAR-γ Signaling
by Alessia Filippone, Giovanna Casili, Sarah Adriana Scuderi, Deborah Mannino, Marika Lanza, Michela Campolo, Irene Paterniti, Anna Paola Capra, Cristina Colarossi, Annalisa Bonasera, Sofia Paola Lombardo, Salvatore Cuzzocrea and Emanuela Esposito
Cancers 2023, 15(1), 217; https://doi.org/10.3390/cancers15010217 - 29 Dec 2022
Cited by 12 | Viewed by 2837
Abstract
New therapeutic approaches are needed to improve the outcome of patients with glioblastoma (GBM). Propionate, a short-chain fatty acid (SCFA), has a potent antiproliferative effect on various tumor cell types. Peroxisome proliferator-activated receptor (PPAR) ligands possess anticancer properties. We aimed to investigate the [...] Read more.
New therapeutic approaches are needed to improve the outcome of patients with glioblastoma (GBM). Propionate, a short-chain fatty acid (SCFA), has a potent antiproliferative effect on various tumor cell types. Peroxisome proliferator-activated receptor (PPAR) ligands possess anticancer properties. We aimed to investigate the PPAR-γ/SCFAs interaction in in vitro and in vivo models of GBM. The U87 cell line was used in the in vitro study and was treated with sodium propionate (SP). U87 cells were silenced by using PPAR-γ siRNA or Ctr siRNA. In the in vivo study, BALB/c nude mice were inoculated in the right flank with 3 × 106 U-87 cells. SP (doses of 30 and 100 mg/kg) and GW9662 (1 mg/kg) were administered. In vitro exposure of GBM to SP resulted in prominent apoptosis activation while the autophagy pathway was promoted by SP treatments by influencing autophagy-related proteins. Knockdown of PPAR-γ sensitized GBM cells and blocked the SP effect. In vivo, SP was able to decrease tumor growth and to resolve GBM tissue features. SP promoted apoptosis and autophagy pathways and tumor cell proliferation leading to cell cycle arrest through a PPAR-γ-dependent mechanism suggesting that the PPAR-γ/SCFAs axis could be targeted for the management of GBM. Full article
(This article belongs to the Special Issue The Role of Autophagy in Brain Tumors)
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15 pages, 7832 KiB  
Article
ONX-0914 Induces Apoptosis and Autophagy with p53 Regulation in Human Glioblastoma Cells
by Hsin-Han Chang, Yi-Hsuan Lin, Tzu-Min Chen, Yu-Ling Tsai, Chien-Rui Lai, Wen-Chiuan Tsai, Yu-Chen Cheng and Ying Chen
Cancers 2022, 14(22), 5712; https://doi.org/10.3390/cancers14225712 - 21 Nov 2022
Cited by 5 | Viewed by 2056
Abstract
Glioblastoma is believed to be one of the most aggressive brain tumors in the world. ONX-0914 (PR957) is a selective inhibitor of proteasome subunit beta type-8 (PSMB8). Previous studies have shown that inhibiting PSMB8 expression in glioblastoma reduces tumor progression. Therefore, this study [...] Read more.
Glioblastoma is believed to be one of the most aggressive brain tumors in the world. ONX-0914 (PR957) is a selective inhibitor of proteasome subunit beta type-8 (PSMB8). Previous studies have shown that inhibiting PSMB8 expression in glioblastoma reduces tumor progression. Therefore, this study aimed to determine whether ONX-0914 has antitumor effects on human glioblastoma. The results indicated that ONX-0914 treatment inhibited survival in LN229, GBM8401, and U87MG glioblastoma cells. Cell cycle analysis showed that ONX-0914 treatment caused cell cycle arrest at the G1 phase and apoptosis in glioblastoma cells. The protein expression of BCL-2 was reduced and PARP was cleaved after ONX-0914 treatment. Furthermore, the levels of p53 and phosphorylated p53 were increased by ONX-0914 treatment in glioblastoma cells. ONX-0914 also induced autophagy in glioblastoma cells. Furthermore, the p53 inhibitor pifithrin attenuated apoptosis but enhanced autophagy caused by ONX-0914. In an orthotopic mouse model, TMZ plus ONX-0914 reduced tumor progression better than the control or TMZ alone. These data suggest that ONX-0914 is a novel therapeutic drug for glioblastoma. Full article
(This article belongs to the Special Issue The Role of Autophagy in Brain Tumors)
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29 pages, 3617 KiB  
Article
Polyethylenimine, an Autophagy-Inducing Platinum-Carbene-Based Drug Carrier with Potent Toxicity towards Glioblastoma Cancer Stem Cells
by Conor McCartin, Candice Dussouillez, Chloé Bernhard, Eric Mathieu, Juliette Blumberger, Monique Dontenwill, Christel Herold-Mende, Ahmed Idbaih, Philippe Lavalle, Stéphane Bellemin-Laponnaz, Antoine Kichler and Sylvie Fournel
Cancers 2022, 14(20), 5057; https://doi.org/10.3390/cancers14205057 - 15 Oct 2022
Cited by 7 | Viewed by 2675
Abstract
The difficulty involved in the treatment of many tumours due to their recurrence and resistance to chemotherapy is tightly linked to the presence of cancer stem cells (CSCs). This CSC sub-population is distinct from the majority of cancer cells of the tumour bulk. [...] Read more.
The difficulty involved in the treatment of many tumours due to their recurrence and resistance to chemotherapy is tightly linked to the presence of cancer stem cells (CSCs). This CSC sub-population is distinct from the majority of cancer cells of the tumour bulk. Indeed, CSCs have increased mitochondrial mass that has been linked to increased sensitivity to mitochondrial targeting compounds. Thus, a platinum-based polyethylenimine (PEI) polymer–drug conjugate (PDC) was assessed as a potential anti-CSC therapeutic since it has previously displayed mitochondrial accumulation. Our results show that CSCs have increased specific sensitivity to the PEI carrier and to the PDC. The mechanism of cell death seems to be necrotic in nature, with an absence of apoptotic markers. Cell death is accompanied by the induction of a protective autophagy. The interference in the balance of this pathway, which is highly important for CSCs, may be responsible for a partial reversion of the stem-like phenotype observed with prolonged PEI and PDC treatment. Several markers also indicate the cell death mode to be capable of inducing an anti-cancer immune response. This study thus indicates the potential therapeutic perspectives of polycations against CSCs. Full article
(This article belongs to the Special Issue The Role of Autophagy in Brain Tumors)
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17 pages, 3514 KiB  
Article
A Selective Histone Deacetylase Inhibitor Induces Autophagy and Cell Death via SCNN1A Downregulation in Glioblastoma Cells
by Hui Hua Chang, Yao-Yuan Chang, Bing-Chen Tsai, Li-Jyun Chen, An-Chi Chang, Jian-Ying Chuang, Po-Wu Gean and Yuan-Shuo Hsueh
Cancers 2022, 14(18), 4537; https://doi.org/10.3390/cancers14184537 - 19 Sep 2022
Cited by 8 | Viewed by 2444
Abstract
Glioblastoma multiforme (GBM) is a grade IV, highly malignant brain tumor. Because of the heterogeneity of GBM, a multitarget drug is a rational strategy for GBM treatment. Histone deacetylase inhibitors (HDACis) regulate the expression of numerous genes involved in cell death, apoptosis, and [...] Read more.
Glioblastoma multiforme (GBM) is a grade IV, highly malignant brain tumor. Because of the heterogeneity of GBM, a multitarget drug is a rational strategy for GBM treatment. Histone deacetylase inhibitors (HDACis) regulate the expression of numerous genes involved in cell death, apoptosis, and tumorigenesis. We found that the HDAC4/HDAC5 inhibitor LMK235 at 0.5 µM significantly reduced the cell viability and colony formation of patient-derived, temozolomide-resistant GBM P#5 TMZ-R, U-87 MG, and T98G cells. Moreover, LMK235 also significantly increased TUBA acetylation, which is an indicator of HDAC inhibition. Interestingly, LMK235 induced MAP1LC3 robust readout and puncta accumulation but did not enhance PARP1 cleavage or the proportion of annexin V-positive cells, suggesting that LMK235-induced cell death occurred via autophagy activation. Further RNA-seq analysis after LMK235 treatment showed that 597 different expression genes compared to control. After bioinformatic analysis by KEGG and STRING, we focused on 34 genes and validated their mRNA expression by qPCR. Further validation showed that 2 µM LMK235 significantly reduced the mRNA and protein expression of SCNN1A. Cell viability of SCNN1A-silenced cells were reduced, but cells were rescued while treated with an autophagy inhibitor bafilomycin A1. Conclusively, SCNN1A plays a role in LMK235-induced autophagy and cell death in GBM cells. Full article
(This article belongs to the Special Issue The Role of Autophagy in Brain Tumors)
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Review

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26 pages, 1506 KiB  
Review
Autophagic-Related Proteins in Brain Gliomas: Role, Mechanisms, and Targeting Agents
by Cristina Pizzimenti, Vincenzo Fiorentino, Mariausilia Franchina, Maurizio Martini, Giuseppe Giuffrè, Maria Lentini, Nicola Silvestris, Martina Di Pietro, Guido Fadda, Giovanni Tuccari and Antonio Ieni
Cancers 2023, 15(9), 2622; https://doi.org/10.3390/cancers15092622 - 5 May 2023
Cited by 8 | Viewed by 2305
Abstract
The present review focuses on the phenomenon of autophagy, a catabolic cellular process, which allows for the recycling of damaged organelles, macromolecules, and misfolded proteins. The different steps able to activate autophagy start with the formation of the autophagosome, mainly controlled by the [...] Read more.
The present review focuses on the phenomenon of autophagy, a catabolic cellular process, which allows for the recycling of damaged organelles, macromolecules, and misfolded proteins. The different steps able to activate autophagy start with the formation of the autophagosome, mainly controlled by the action of several autophagy-related proteins. It is remarkable that autophagy may exert a double role as a tumour promoter and a tumour suppressor. Herein, we analyse the molecular mechanisms as well as the regulatory pathways of autophagy, mainly addressing their involvement in human astrocytic neoplasms. Moreover, the relationships between autophagy, the tumour immune microenvironment, and glioma stem cells are discussed. Finally, an excursus concerning autophagy-targeting agents is included in the present review in order to obtain additional information for the better treatment and management of therapy-resistant patients. Full article
(This article belongs to the Special Issue The Role of Autophagy in Brain Tumors)
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