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Special Issue "Apoptosis and Autophagy: The Double Edge in Cancer Development and Progression and in Other Human Diseases 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2020).

Special Issue Editors

Prof. Dr. Michele Caraglia
Website
Guest Editor
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy
Interests: cancer; miRNAs; nanotechnology; drug delivery; nano sensors; long non-coding RNA; signal transduction; isoprenylation and cancer; aminobisphosphonates; glioblastoma; prostate cancer; hepatocellular cancer; signal transduction; Ras; interferons
Special Issues and Collections in MDPI journals
Prof. Dr. Maria Luisa Balestrieri
Website
Guest Editor
Department of Precision Medicine, School of Medicine, University of Campania “Luigi Vanvitelli”, Naples, Italy
Interests: aging, oxidative stress, nitric oxide, endothelial cells, endothelial progenitor cells, angiogenesis, inflammation, cell senescence, apoptosis, atherosclerosis, diabetes, endothelial dysfunction, sirtuins and cardiovascular disease; natural products, betaines, health, bioactive compounds, free radicals, antioxidants, ergothioneine; cell cycle, cancer-related biochemical pathways, cell proliferation, senescence, cancer cell death, epigenetic regulation, sirtuins and cancer
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announced the continuation of our Special Issue “Apoptosis and Autophagy: The Double Edge in Cancer Development and Progression and in Other Human Diseases”, with a second edition.

The mechanisms of cell death have a pivotal role in the determination of the fate of normal and cancer cells in a multicellular organism. The disruption of these mechanisms is at the core of the development of inflammatory and tumor diseases, and knowledge of the molecular components altered in specific illnesses can be useful in the design of new therapeutic strategies for the treatment of human cancers as well as of inflammatory diseases. Two of the most known cell death mechanisms are apoptosis and autophagy, which are differently-involved in the regulation of tumor cell proliferation and metastasization. These mechanisms are often opposite, and autophagy is described as an escape mechanism from apoptotic occurrence, representing a protective effect of tumor cells to anti-cancer agents or hypoxic conditions, both of which are deleterious for cancer progression. On the other hand, some anti-cancer agents can induce autophagy during the repression of tumor proliferation. In this way, autophagy can become a marker of cancer response to treatment. The existence of specific tumor conditions can determine the functional role of autophagy in cancer tissues. The interaction between autophagy and apoptosis occurs through the cross-talk of the respective molecular mechanisms that are able to influence each other in a tunable way. A role for apoptosis and autophagy in the regulation of normal tissue development and differentiation is also emerging. Therefore, apoptosis and autophagy also regulate the physiological mechanisms of several organs (i.e., liver and ovary), and are involved in the occurrence of several diseases, based on either a development defect or a chronic inflammatory status. The intervention on the programmed cell death with specific agents can be a new strategy for the treatment of these kinds of diseases.

This Issue of the International Journal of Molecular Sciences will focus on the recent advances in “Apoptosis and Autophagy: The Double Edge in Cancer Development and Progression and in Other Human Diseases 2.0”, including new insights into the molecular mechanisms of apoptosis, autophagy, and other programmed cell death mechanisms (i.e., senescence), and their correlations with the control of cancer growth, metastasization, tissue development, and inflammation. Moreover, emerging data on the natural or synthetic modulators of apoptosis and autophagy in relation to new therapeutic strategies are welcome.

Prof. Dr. Michele Caraglia
Prof. Dr. Maria Luisa Balestrieri
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • autophagy
  • cancer
  • miRNA
  • long non-coding RNAs
  • senescence
  • inflammation
  • therapeutics

Published Papers (3 papers)

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Research

Open AccessArticle
TLR3 Expression Induces Apoptosis in Human Non-Small-Cell Lung Cancer
Int. J. Mol. Sci. 2020, 21(4), 1440; https://doi.org/10.3390/ijms21041440 - 20 Feb 2020
Abstract
The prognostic value of Toll-like receptor 3 (TLR3) is debated in cancer, differing between tumor types, methods, and cell types. We recently showed for the first time that TLR3 expression on early stage non-small-cell lung cancer (NSCLC) results associated with a good prognosis. [...] Read more.
The prognostic value of Toll-like receptor 3 (TLR3) is debated in cancer, differing between tumor types, methods, and cell types. We recently showed for the first time that TLR3 expression on early stage non-small-cell lung cancer (NSCLC) results associated with a good prognosis. Here, we provide experimental evidences explaining the molecular reason behind TLR3’s favorable prognostic role. We demonstrated that TLR3 activation in vitro induces apoptosis in lung cancer cell lines and, accordingly, that TLR3 expression is associated with caspase-3 activation in adenocarcinoma NSCLC specimens, both evaluated by immunohistochemistry. Moreover, we showed that TLR3 expression on cancer cells contributes to activate the CD103+ lung dendritic cell subset, that is specifically associated with processing of antigens derived from apoptotic cells and their presentation to CD8+ T lymphocytes. These findings point to the relevant role of TLR3 expression on lung cancer cells and support the use of TLR3 agonists in NSCLC patients to re-activate local innate immune response. Full article
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Open AccessCommunication
Anti-Apoptotic and Anti-Oxidant Proteins in Glioblastomas: Immunohistochemical Expression of Beclin and DJ-1 and Its Correlation with Prognosis
Int. J. Mol. Sci. 2019, 20(16), 4066; https://doi.org/10.3390/ijms20164066 - 20 Aug 2019
Abstract
DJ-1 deglycase is a protein with anti-oxidative and anti-apoptotic properties and its role in oncogenesis is controversial. Indeed in primary breast cancer and non-small-cell lung carcinoma, its higher expression was shown in more aggressive tumors while in other neoplasms (e.g., pancreatic adenocarcinoma), higher [...] Read more.
DJ-1 deglycase is a protein with anti-oxidative and anti-apoptotic properties and its role in oncogenesis is controversial. Indeed in primary breast cancer and non-small-cell lung carcinoma, its higher expression was shown in more aggressive tumors while in other neoplasms (e.g., pancreatic adenocarcinoma), higher expression was related to better prognosis. Beclin has a relevant role in autophagy and cellular death regulation, processes that are well known to be impaired in neoplastic cells. DJ-1 shows the ability to modulate signal transduction. It can modulate autophagy through many signaling pathways, a process that can mediate either cell survival or cell death depending on the circumstances. Previously, it has been suggested that the involvement of DJ-1 in autophagy regulation may play a role in tumorigenesis. The aim of our study was to investigate the link between DJ-1 and Beclin-1 in glioblastoma through the immunohistochemical expression of such proteins and to correlate the data obtained with prognosis. Protein expression was assessed by immunohistochemistry and the immunoscores were correlated with clinicopathologic parameters. Kaplan–Meier survival curves were generated. A statistically significant association between DJ-1 score and recurrence (p = 0.0189) and between the former and Isocitrate Dehydrogenase 1 (IDH1) mutation (p = 0.0072) was observed. Kaplan–Meier survival curve analysis revealed that a higher DJ-1 score was associated with longer overall survival (p = 0.0253, ĸ2 = 5.005). Furthermore, an unexpected direct correlation (p = 0.0424, r = 0.4009) between DJ-1 and Beclin score was evident. The most significant result of the present study was the evidence of high DJ-1 expression in IDH-mutant tumors and in cases with longer overall survival. This finding could aid, together with IDH1, in the identification of glioblastomas with better prognosis. Full article
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Open AccessArticle
A Hydroquinone-Based Derivative Elicits Apoptosis and Autophagy via Activating a ROS-Dependent Unfolded Protein Response in Human Glioblastoma
Int. J. Mol. Sci. 2019, 20(15), 3836; https://doi.org/10.3390/ijms20153836 - 06 Aug 2019
Cited by 2
Abstract
5-Lipoxygenase (5-LO) has been reported to be highly expressed in brain tumors and to promote glioma cell proliferation. Therefore, we investigated the anticancer activity of the novel 5-LO inhibitor derivative 3-tridecyl-4,5-dimethoxybenzene-1,2-diol hydroquinone (EA-100C red) on glioblastoma (GBM) cell growth. Cell viability was evaluated [...] Read more.
5-Lipoxygenase (5-LO) has been reported to be highly expressed in brain tumors and to promote glioma cell proliferation. Therefore, we investigated the anticancer activity of the novel 5-LO inhibitor derivative 3-tridecyl-4,5-dimethoxybenzene-1,2-diol hydroquinone (EA-100C red) on glioblastoma (GBM) cell growth. Cell viability was evaluated by MTT assay. The effects of the compound on apoptosis, oxidative stress and autophagy were assessed by flow cytometry (FACS). The mode of action was confirmed by Taqman apoptosis array, Real Time qPCR, confocal microscopy analysis and the western blotting technique. Our results showed that EA-100C Red had a higher anti-proliferative effect on LN229 as compared to U87MG cells. The compound induced a significant increase of apoptosis and autophagy and up-regulated pro-apoptotic genes (Bcl3, BNIP3L, and NFKBIA) in both GBM cell lines. In this light, we studied the effects of EA-100C red on the expression of CHOP and XBP1, that are implicated in ER-stress-mediated cell death. In summary, our findings revealed that EA-100C red induced ER stress-mediated apoptosis associated to autophagy in GBM cells through CHOP and Beclin1 up-regulation and activation of caspases 3, 9, JNK and NF-kappaB pathway. On these bases, EA-100C red could represent a promising compound for anti-cancer treatment. Full article
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