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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 6124

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Dr. Ming-Ju Hsieh

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Guest Editor

Oral Cancer Research Center, Changhua Christian Hospital, Changhua 500, Taiwan
Interests: apoptosis; autophagy; metastasis; anti-cancer; nature compound; cell biochemistry
Special Issues, Collections and Topics in MDPI journals

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Dear Colleagues,

Autophagy is a normal process in which a cell destroys proteins and other substances in its cytoplasm. Autophagy may prevent normal cells from developing into cancer cells, but it may also protect cancer cells by destroying anticancer drugs or substances taken up by them. Autophagy is a process by which cellular material is degraded by lysosomes or vacuoles and recycled. Several autophagy pathways operate within a cell, including macroautophagy, microautophagy and chaperone-mediated autophagy. We welcome research articles and review papers focused on autophagy in cancer, from basic translational science studies to clinical research.

Dr. Ming-Ju Hsieh
Guest Editor

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

autophagy
lysosomes
macroautophagy
microautophagy
chaperone-mediated autophagy

Published Papers (5 papers)

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Research

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17 pages, 12029 KiB

Open AccessArticle

COPI Vesicle Disruption Inhibits Mineralization via mTORC1-Mediated Autophagy

by Jiaming Nie, Shaoyang Ma, Yuchen Zhang, Shuchen Yu, Jiajia Yang, Ang Li and Dandan Pei

Int. J. Mol. Sci. 2024, 25(1), 339; https://doi.org/10.3390/ijms25010339 - 26 Dec 2023

Viewed by 711

Abstract

Bone mineralization is a sophisticated regulated process composed of crystalline calcium phosphate and collagen fibril. Autophagy, an evolutionarily conserved degradation system, whereby double-membrane vesicles deliver intracellular macromolecules and organelles to lysosomes for degradation, has recently been shown to play an essential role in mineralization. However, the formation of autophagosomes in mineralization remains to be determined. Here, we show that Coat Protein Complex I (COPI), responsible for Golgi-to-ER transport, plays a pivotal role in autophagosome formation in mineralization. COPI vesicles were increased after osteoinduction, and COPI vesicle disruption impaired osteogenesis. Mechanistically, COPI regulates autophagy activity via the mTOR complex 1 (mTORC1) pathway, a key regulator of autophagy. Inhibition of mTOR1 rescues the impaired osteogenesis by activating autophagy. Collectively, our study highlights the functional importance of COPI in mineralization and identifies COPI as a potential therapeutic target for treating bone-related diseases. Full article

(This article belongs to the Special Issue Recent Research on Autophagy)

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13 pages, 2944 KiB

Open AccessArticle

Integrated Multi-Omics Analyses Reveal That Autophagy-Mediated Cellular Metabolism Is Required for the Initiation of Pollen Germination

by Xuemei Zhou, Qiuyu Zhang, Yuliang Zhao, Shanshan Ding and Guang-Hui Yu

Int. J. Mol. Sci. 2023, 24(19), 15014; https://doi.org/10.3390/ijms241915014 - 09 Oct 2023

Viewed by 806

Abstract

Autophagy is an evolutionarily conserved mechanism for degrading and recycling various cellular components, functioning in both normal development and stress conditions. This process is tightly regulated by a set of autophagy-related (ATG) proteins, including ATG2 in the ATG9 cycling system and ATG5 in the ATG12 conjugation system. Our recent research demonstrated that autophagy-mediated compartmental cytoplasmic deletion is essential for pollen germination. However, the precise mechanisms through which autophagy regulates pollen germination, ensuring its fertility, remain largely unknown. Here, we applied multi-omics analyses, including transcriptomic and metabolomic approaches, to investigate the downstream pathways of autophagy in the process of pollen germination. Although ATG2 and ATG5 play similar roles in regulating pollen germination, high-throughput transcriptomic analysis reveals that silencing ATG5 has a greater impact on the transcriptome than silencing ATG2. Cross-comparisons of transcriptome and proteome analysis reveal that gene expression at the mRNA level and protein level is differentially affected by autophagy. Furthermore, high-throughput metabolomics analysis demonstrates that pathways related to amino acid metabolism and aminoacyl-tRNA biosynthesis were affected by both ATG2 and ATG5 silencing. Collectively, our multi-omics analyses reveal the central role of autophagy in cellular metabolism, which is critical for initiating pollen germination and ensuring pollen fertility. Full article

(This article belongs to the Special Issue Recent Research on Autophagy)

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15 pages, 4042 KiB

Open AccessArticle

The Small-Molecule Enhancers of Autophagy AUTEN-67 and -99 Delay Ageing in Drosophila Striated Muscle Cells

by Marcell Komlós, Janka Szinyákovics, Gergő Falcsik, Tímea Sigmond, Bálint Jezsó, Tibor Vellai and Tibor Kovács

Int. J. Mol. Sci. 2023, 24(9), 8100; https://doi.org/10.3390/ijms24098100 - 30 Apr 2023

Cited by 2 | Viewed by 1494

Abstract

Autophagy (cellular self-degradation) plays a major role in maintaining the functional integrity (homeostasis) of essentially all eukaryotic cells. During the process, superfluous and damaged cellular constituents are delivered into the lysosomal compartment for enzymatic degradation. In humans, age-related defects in autophagy have been linked to the incidence of various age-associated degenerative pathologies (e.g., cancer, neurodegenerative diseases, diabetes, tissue atrophy and fibrosis, and immune deficiency) and accelerated ageing. Muscle mass decreases at detectable levels already in middle-aged patients, and this change can increase up to 30–50% at age 80. AUTEN-67 and -99, two small-molecule enhancers of autophagy with cytoprotective and anti-ageing effects have been previously identified and initially characterized. These compounds can increase the life span in wild-type and neurodegenerative model strains of the fruit fly Drosophila melanogaster. Adult flies were treated with these AUTEN molecules via feeding. Fluorescence and electron microscopy and Western blotting were used to assess the level of autophagy and cellular senescence. Flying tests were used to measure the locomotor ability of the treated animals at different ages. In the current study, the effects of AUTEN-67 and -99 were observed on striated muscle cells using the Drosophila indirect flight muscle (IFM) as a model. The two molecules were capable of inducing autophagy in IFM cells, thereby lowering the accumulation of protein aggregates and damaged mitochondria, both characterizing muscle ageing. Furthermore, the two molecules significantly improved the flying ability of treated animals. AUTEN-67 and -99 decrease the rate at which striated muscle cells age. These results may have a significant medical relevance that could be further examined in mammalian models. Full article

(This article belongs to the Special Issue Recent Research on Autophagy)

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Review

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19 pages, 3403 KiB

Open AccessReview

Autophagy as a Target for Non-Immune Intrinsic Functions of Programmed Cell Death-Ligand 1 in Cancer

by Blanca Estela García-Pérez, Christian Pérez-Torres, Shantal Lizbeth Baltierra-Uribe, Juan Castillo-Cruz and Nayeli Shantal Castrejón-Jiménez

Int. J. Mol. Sci. 2023, 24(19), 15016; https://doi.org/10.3390/ijms241915016 - 09 Oct 2023

Cited by 2 | Viewed by 1527

Abstract

Autophagy is a catabolic process that is essential to the maintenance of homeostasis through the cellular recycling of damaged organelles or misfolded proteins, which sustains energy balance. Additionally, autophagy plays a dual role in modulating the development and progression of cancer and inducing a survival strategy in tumoral cells. Programmed cell death-ligand 1 (PD-L1) modulates the immune response and is responsible for maintaining self-tolerance. Because tumor cells exploit the PD-L1–PD-1 interaction to subvert the immune response, immunotherapy has been developed based on the use of PD-L1-blocking antibodies. Recent evidence has suggested a bidirectional regulation between autophagy and PD-L1 molecule expression in tumor cells. Moreover, the research into the intrinsic properties of PD-L1 has highlighted new functions that are advantageous to tumor cells. The relationship between autophagy and PD-L1 is complex and still not fully understood; its effects can be context-dependent and might differ between tumoral cells. This review refines our understanding of the non-immune intrinsic functions of PD-L1 and its potential influence on autophagy, how these could allow the survival of tumor cells, and what this means for the efficacy of anti-PD-L1 therapeutic strategies. Full article

(This article belongs to the Special Issue Recent Research on Autophagy)

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27 pages, 2433 KiB

Open AccessReview

Autophagy Modulation as a Potential Therapeutic Strategy in Osteosarcoma: Current Insights and Future Perspectives

by Sergio Almansa-Gómez, Francisco Prieto-Ruiz, José Cansado and Marisa Madrid

Int. J. Mol. Sci. 2023, 24(18), 13827; https://doi.org/10.3390/ijms241813827 - 07 Sep 2023

Viewed by 1122

Abstract

Autophagy, the process that enables the recycling and degradation of cellular components, is essential for homeostasis, which occurs in response to various types of stress. Autophagy plays an important role in the genesis and evolution of osteosarcoma (OS). The conventional treatment of OS has limitations and is not always effective at controlling the disease. Therefore, numerous researchers have analyzed how controlling autophagy could be used as a treatment or strategy to reverse resistance to therapy in OS. They highlight how the inhibition of autophagy improves the efficacy of chemotherapeutic treatments and how the promotion of autophagy could prove positive in OS therapy. The modulation of autophagy can also be directed against OS stem cells, improving treatment efficacy and preventing cancer recurrence. Despite promising findings, future studies are needed to elucidate the molecular mechanisms of autophagy and its relationship to OS, as well as the mechanisms underlying the functioning of autophagic modulators. Careful evaluation is required as autophagy modulation may have adverse effects on normal cells, and the optimization of autophagic modulators for use as drugs in OS is imperative. Full article

(This article belongs to the Special Issue Recent Research on Autophagy)

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