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Life
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Autophagy and Cancer 2021
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Autophagy and Cancer 2021

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 20416

Special Issue Editors

Dr. Evangelos Koustas

E-Mail Website
Guest Editor
Molecular Oncology Unit, Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece
Interests: oncology; medicine; cancer biology; autophagy; molecular science
Special Issues, Collections and Topics in MDPI journals
Dr. Panagiotis Sarantis

E-Mail Website
Guest Editor
Molecular Oncology Unit, Department of Biological Chemistry, National and Kapodistrian University of Athens, Athens, Greece
Interests: Molecular Oncology Unit, Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy as a primary homeostatic and catabolic process is responsible for the degradation and recycling of proteins and cellular components. The mechanism of autophagy has a crucial role in several cellular functions and its dysregulation is associated with tumorigenesis, tumor–stroma interactions, and resistance to cancer therapy. A growing body of evidence suggests that autophagy is also a key regulator of the tumor microenvironment and cellular immune response in different types of cancer. A growing body of evidence suggests that autophagy mainly acts as a tumor suppressor during the early stage of tumorigenesis and tumor promotion in already established tumors at the late stage of tumorigenesis.

This Special Issue will investigate the role of autophagy in different cancer types. It will focus on different circumstances that autophagy is implicated in tumorigenesis and is expected to provide novel and more efficient therapeutic protocols for cancer patients. Furthermore, patient selection based on the basic levels of autophagy biomarkers such as ATGs, Beclin-1, LC3, p62, and MicroRNAs could pave the way for better chemotherapeutic treatment with autophagy modulators. Developing autophagy modulators with minimal cross-talk with other agents will be challenging and crucial to make autophagy a successful target strategy for cancer therapy. In light of the results, it is a huge challenge to better understand the impact and the molecular mechanism of autophagy in tumorigenesis to translate preclinical data into clinical practice successfully.

Dr. Evangelos Koustas
Dr. Panagiotis Sarantis
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. Life is an international peer-reviewed open access monthly 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 2600 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

  • autophagy
  • cancer
  • tumor microenvironment
  • immunotherapy
  • biomarkers

Related Special Issue

Published Papers (7 papers)

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Research

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15 pages, 6579 KiB  
Article
Identification of Compound CB-2 as a Novel Late-Stage Autophagy Inhibitor Exhibits Inhibitory Potency against A549 Cells
by Zhihui Liu, Lu Zhang, Yachao Liu, Hanxiao Zhang, Jingxuan Chen, Gaoqing Feng, Peichang Yang, Fangfang Sha, Liuqing Cui and Gangchun Sun
Life 2021, 11(8), 865; https://doi.org/10.3390/life11080865 - 23 Aug 2021
Cited by 3 | Viewed by 2025
Abstract
Autophagy has been recognized as a stress tolerance mechanism that maintains cell viability, which contributes to tumor progression, dormancy, and treatment resistance. The inhibition of autophagy in cancer has the potential to improve the therapeutic efficacy. It is therefore of great significance to [...] Read more.
Autophagy has been recognized as a stress tolerance mechanism that maintains cell viability, which contributes to tumor progression, dormancy, and treatment resistance. The inhibition of autophagy in cancer has the potential to improve the therapeutic efficacy. It is therefore of great significance to search for new autophagy inhibitors. In the present study, after screening a series of curcumin derivatives synthesized in our laboratory, (E)-3-((E)-4-chlorobenzylidene)-5-((5-methoxy-1H-indol-3-yl)methylene)-1-methylpiperidin-4-one (CB-2) was selected as a candidate for further study. We found that CB-2 increased the LC3B-II and SQSTM1 levels associated with the accumulation of autophagosomes in non-small cell lung cancer (NSCLC) A549 cells. The increased level of LC3B-II induced by CB-2 was neither eliminated when autophagy initiation was suppressed by wortmannin nor further increased when autophagosome degradation was inhibited by chloroquine (CQ). CB-2 enhanced the accumulation of LC3B-II under starvation conditions. Further studies revealed that CB-2 did not affect the levels of the key proteins involved in autophagy induction but significantly blocked the fusion of autophagosomes with lysosomes. High-dose CB-2 induced the apoptosis and necrosis of A549 cells, while a lower dose of CB-2 mainly impaired the migrative capacity of A549 cells, which only slightly induced cell apoptosis. CB-2 increased the levels of mitochondrial-derived reactive oxygen species (ROS) while decreasing the mitochondrial membrane potential (MMP). Scavenging ROS via N-acetylcysteine (NAC) reversed CB-2-induced autophagy inhibition and its inhibitory effect against A549 cells. In conclusion, CB-2 serves as a new late-stage autophagy inhibitor, which has a strong inhibitory potency against A549 cells. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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17 pages, 3710 KiB  
Article
Identification of Autophagy- and Ferroptosis-Related lncRNAs Functioned through Immune-Related Pathways in Head and Neck Squamous Carcinoma
by Qi Guo, Xuehan Zhang, Tao Shen and Xiangting Wang
Life 2021, 11(8), 835; https://doi.org/10.3390/life11080835 - 16 Aug 2021
Cited by 12 | Viewed by 3258
Abstract
The interplay between autophagy and ferroptosis has been highlighted as an important event to decide cancer cell fate. However, the underlying mechanisms remain largely unclear. In this study, we systematically explored the expression, prognostic value and functional roles of lncRNA in autophagy and [...] Read more.
The interplay between autophagy and ferroptosis has been highlighted as an important event to decide cancer cell fate. However, the underlying mechanisms remain largely unclear. In this study, we systematically explored the expression, prognostic value and functional roles of lncRNA in autophagy and ferroptosis. By a set of bioinformatics analyses, we identified 363 autophagy- and ferroptosis-related lncRNAs (AF-lncRNAs) and found 17 of them are dramatically related to the prognosis of head and neck squamous cell carcinoma (HNSC) patients, named as prognosis-related AF-lncRNAs (PAF-lncRNAs). Based on six key PAF-lncRNAs, a risk score model was developed and used to categorize the TCGA-retrieved HNSC patients into two groups (high-risk vs. low-risk). Functional analysis showed the differentially expressed genes (DEGs) between the two groups were mainly enriched in immune-related pathways and regulated by a PAF-lncRNA-directed ceRNA (competitive endogenous RNA) network. Combined with a variety of immune infiltration analyses, we also found a decreased landscape of immune cell infiltration in high-risk groups. Together, by revealing PAF-lncRNAs with tumor prognostic features functioned through immune-related pathways, our work would contribute to show the pathogenesis of a lncRNA-directed interplay among autophagy, ferroptosis and tumor immunity in HNSC and to develop potential prognostic biomarkers and targets for tumor immunotherapy. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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12 pages, 4168 KiB  
Article
Steroidal Saponins Isolated from the Rhizome of Dioscorea tokoro Inhibit Cell Growth and Autophagy in Hepatocellular Carcinoma Cells
by Shinya Okubo, Tomoe Ohta, Yukihiro Shoyama and Takuhiro Uto
Life 2021, 11(8), 749; https://doi.org/10.3390/life11080749 - 26 Jul 2021
Cited by 11 | Viewed by 2148
Abstract
Our preliminary screening identified an extract from the rhizome of Dioscorea tokoro, which strongly suppressed the proliferation of HepG2 hepatocellular carcinoma cells and inhibited autophagy. This study aimed to isolate active compounds from the rhizome of D. tokoro that exert antiproliferative effects [...] Read more.
Our preliminary screening identified an extract from the rhizome of Dioscorea tokoro, which strongly suppressed the proliferation of HepG2 hepatocellular carcinoma cells and inhibited autophagy. This study aimed to isolate active compounds from the rhizome of D. tokoro that exert antiproliferative effects and inhibit autophagy. The bioassay-guided fractionation of the active fraction led to the isolation of two spirostan-type steroidal saponins, dioscin (1) and yamogenin 3-O-α-l-rhamnopyranosyl (1→4)-O-α-l-rhamnopyranosyl(1→2)-β-d-glucopyranoside (2), and the frostane-type steroidal saponin protodioscin (3) from the n-BuOH fraction. Furthermore, acid hydrolysis of 1 and 2 produced the aglycones diosgenin (4) and yamogenin (5), respectively. Compounds 1–5 suppressed proliferation of HepG2 cells. The analysis of structure-activity relationships indicated that the 25(R)-conformation, structures with a sugar moiety, and the spirostan-type aglycone moiety contributed to antiproliferative activity. Analysis of autophagy-related proteins demonstrated that 1–3 clearly increased the levels of both LC3-II and p62, implying that 1–3 deregulate the autophagic pathway by blocking autophagic flux, which results in p62 and LC3-II accumulation. In contrast, 1–3 did not significantly affect caspase-3 activation and PARP cleavage, suggesting that the antiproliferative activity of 1–3 occurred independently of caspase-3-mediated apoptosis. In summary, our study showed that 1–3, active compounds in the rhizome of D. tokoro, suppressed cell proliferation and autophagy, and might be potential agents for autophagy research and cancer chemoprevention. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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Review

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16 pages, 1258 KiB  
Review
The Implication of Autophagy in Gastric Cancer Progression
by Evangelos Koustas, Eleni-Myrto Trifylli, Panagiotis Sarantis, Nikolaos I. Kontolatis, Christos Damaskos, Nikolaos Garmpis, Christos Vallilas, Anna Garmpi, Athanasios G. Papavassiliou and Michalis V. Karamouzis
Life 2021, 11(12), 1304; https://doi.org/10.3390/life11121304 - 27 Nov 2021
Cited by 9 | Viewed by 2192
Abstract
Gastric cancer is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. The three entirely variable entities have distinct epidemiology, molecular characteristics, prognosis, and strategies for clinical management. However, many gastric tumors appear to be resistant to current [...] Read more.
Gastric cancer is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. The three entirely variable entities have distinct epidemiology, molecular characteristics, prognosis, and strategies for clinical management. However, many gastric tumors appear to be resistant to current chemotherapeutic agents. Moreover, a significant number of gastric cancer patients, with a lack of optimal treatment strategies, have reduced survival. In recent years, multiple research data have highlighted the importance of autophagy, an essential catabolic process of cytoplasmic component digestion, in cancer. The role of autophagy as a tumor suppressor or tumor promoter mechanism remains controversial. The multistep nature of the autophagy process offers a wide array of targetable points for designing novel chemotherapeutic strategies. The purpose of this review is to summarize the current knowledge regarding the interplay between gastric cancer development and the autophagy process and decipher the role of autophagy in this kind of cancer. A plethora of different agents that direct or indirect target autophagy may be a novel therapeutic approach for gastric cancer patients. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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14 pages, 1479 KiB  
Review
Crosstalk between Autophagy and Inflammatory Processes in Cancer
by Eun-Ji Lee, Hyun-Jeong Kim, Min Sik Choi and Ji-Eun Chang
Life 2021, 11(9), 903; https://doi.org/10.3390/life11090903 - 30 Aug 2021
Cited by 11 | Viewed by 3052
Abstract
Inflammation is an adaptive response to tissue injury, which is a critical process in order to restore tissue functionality and homeostasis. The association between inflammation and cancer has been a topic of interest for many years, not only inflammatory cells themselves but also [...] Read more.
Inflammation is an adaptive response to tissue injury, which is a critical process in order to restore tissue functionality and homeostasis. The association between inflammation and cancer has been a topic of interest for many years, not only inflammatory cells themselves but also the chemokines and cytokines they produce, which affect cancer development. Autophagy is an intracellular self-degradative process providing elimination of damaged or dysfunctional organelles under stressful conditions such as nutrient deficiency, hypoxia, or chemotherapy. Interestingly, the signaling pathways that are involved in cancer-associated inflammation may regulate autophagy as well. These are (1) the toll-like receptor (TLR) signaling cascade, (2) the reactive oxygen species (ROS) signaling pathway, (3) the inflammatory cytokine signaling pathway, and (4) the IκB kinase (IKK)/Nuclear factor-κB (NF-κB) signaling axis. Moreover, the studies on the context-specific functions of autophagy during inflammatory responses in cancer will be discussed here. On that basis, we focus on autophagy inhibitors and activators regulating inflammatory process in cancer as useful candidates for enhancing anticancer effects. This review summarizes how the autophagic process regulates these key inflammatory processes and vice versa in various cancers. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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19 pages, 4676 KiB  
Review
Autophagy Modulators in Cancer: Focus on Cancer Treatment
by Hye Jin Nam
Life 2021, 11(8), 839; https://doi.org/10.3390/life11080839 - 17 Aug 2021
Cited by 13 | Viewed by 2753
Abstract
Uncontrolled autophagy has been associated with the development and progression of various cancers that are resistant to cancer therapy. Therefore, many efforts to modulate uncontrolled autophagy as a cancer treatment have been attempted, from basic science to clinical trials. However, it remains difficult [...] Read more.
Uncontrolled autophagy has been associated with the development and progression of various cancers that are resistant to cancer therapy. Therefore, many efforts to modulate uncontrolled autophagy as a cancer treatment have been attempted, from basic science to clinical trials. However, it remains difficult to equally apply autophagy modulators to cancer therapy because autophagy is a double-edged sword in cancer: it can be tumor-suppressive or tumor-protective. Therefore, the precise mechanisms of autophagy modulators and their varied responsiveness to each cancer type should be addressed in detail. This study will describe the precise mechanisms of developing various autophagy modulators, their current therapeutic applications and future perspectives. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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17 pages, 1239 KiB  
Review
The Role of Autophagy Modulated by Exercise in Cancer Cachexia
by Julia Windi Gunadi, Ariyani Sudhamma Welliangan, Ray Sebastian Soetadji, Diana Krisanti Jasaputra and Ronny Lesmana
Life 2021, 11(8), 781; https://doi.org/10.3390/life11080781 - 2 Aug 2021
Cited by 6 | Viewed by 3447
Abstract
Cancer cachexia is a syndrome experienced by many patients with cancer. Exercise can act as an autophagy modulator, and thus holds the potential to be used to treat cancer cachexia. Autophagy imbalance plays an important role in cancer cachexia, and is correlated to [...] Read more.
Cancer cachexia is a syndrome experienced by many patients with cancer. Exercise can act as an autophagy modulator, and thus holds the potential to be used to treat cancer cachexia. Autophagy imbalance plays an important role in cancer cachexia, and is correlated to skeletal and cardiac muscle atrophy and energy-wasting in the liver. The molecular mechanism of autophagy modulation in different types of exercise has not yet been clearly defined. This review aims to elaborate on the role of exercise in modulating autophagy in cancer cachexia. We evaluated nine studies in the literature and found a potential correlation between the type of exercise and autophagy modulation. Combined exercise or aerobic exercise alone seems more beneficial than resistance exercise alone in cancer cachexia. Looking ahead, determining the physiological role of autophagy modulated by exercise will support the development of a new medical approach for treating cancer cachexia. In addition, the harmonization of the exercise type, intensity, and duration might play a key role in optimizing the autophagy levels to preserve muscle function and regulate energy utilization in the liver. Full article
(This article belongs to the Special Issue Autophagy and Cancer 2021)
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