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Cells
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Molecular Targets for Autophagy in Cancer Treatment
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Molecular Targets for Autophagy in Cancer Treatment

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 9043

Special Issue Editors

Dr. Yong Li

E-Mail Website
Guest Editor
Baylor College of Medicine, Houston, TX, USA
Interests: cancer biology; immunology; inflammation
Dr. Ashish Tyagi

E-Mail Website
Guest Editor
College of Pharmacy, Texas A&M University, College Station, TX 77843, USA
Interests: cell culture; western blot analysis; immunofluorescence; cloning; DNA extraction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is an evolutionally conserved, lysosomal-dependent process that maintains cellular homeostasis by recycling damaged cellular components. This fundamental process helps cells meet metabolic needs under stressful conditions, such as nutrient deprivation and hypoxia. Autophagy plays a paradoxical role in cancer cells, where it may promote or suppress tumorigenesis depending on the cell type or tumorigenesis stage. Hence, understanding the fundamental role of autophagy in cancer cells is critical to therapeutic development. This Special Issue invites original research or review articles focused on identifying autophagy modulators (inhibitors or inducers), their molecular mode of action, and their potential application in cancer therapy.

Dr. Yong Li
Dr. Ashish Tyagi
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. Cells 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 2700 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
  • tumor progression
  • molecular targets
  • autophagy activators and inhibitors
  • cancer therapy
  • tumor sensitization

Published Papers (3 papers)

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Research

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22 pages, 10650 KiB  
Article
High Fat-High Fructose Diet Elicits Hypogonadotropism Culminating in Autophagy-Mediated Defective Differentiation of Ovarian Follicles
by Chalikkaran Thilakan Rejani, Ajit Kumar Navin, Thekkey Madathil Valappil Mumthaz and Venugopal Bhuvarahamurthy
Cells 2022, 11(21), 3447; https://doi.org/10.3390/cells11213447 - 31 Oct 2022
Cited by 2 | Viewed by 2470
Abstract
Pituitary gonadotropins directly govern ovarian functions, which are in turn regulated by the ovarian steroid hormones. The precise interplay of gonadotropins and steroid hormones is critical for follicle growth and differentiation. Furthermore, autophagy regulates ovarian follicle differentiation. However, how the high-fat-high fructose (HFD-HF) [...] Read more.
Pituitary gonadotropins directly govern ovarian functions, which are in turn regulated by the ovarian steroid hormones. The precise interplay of gonadotropins and steroid hormones is critical for follicle growth and differentiation. Furthermore, autophagy regulates ovarian follicle differentiation. However, how the high-fat-high fructose (HFD-HF) diet regulates gonadotropins and facilitates autophagy-mediated follicular differentiation in the ovary is obscure. We fed prepubertal rats (PND 25) an HFD-HF diet until PND 90. The results showed diminished adenohypophyseal GnRHR, PR, and aromatase expression, whereas AR, ERα, PRLR, and inhibin were augmented, resulting in gonadotropins decline. Interestingly, autophagy biomarkers, Beclin-1, ATG5, ATG12, LC3-II, and LAMP1 were reduced but SQSTM1/p62 was augmented in the ovaries of HFD-HF-fed rats, causing autolysosome to aggregation. The diet altered T, E2, P4, PRL, and their receptors status in the ovary, disturbed estrous cyclicity, and delayed vaginal opening. Ovarian histomorphology exhibited numerous cystic and atretic follicles, along with disturbed follicular maturation and ovulation. Moreover, the reduction of FSHR; steroidogenic proteins; receptor proteins AR, ERβ, PR; and signaling proteins Wnt2 and β-catenin was also noticed in the ovary, whereas PRLR, inhibin, and pGSK3β were augmented. In conclusion, exposure to a prepubertal HFD-HF diet leads to hypogonadotropism and the autophagy-mediated defective differentiation of ovarian follicles, abating fertility in adult rats. Full article
(This article belongs to the Special Issue Molecular Targets for Autophagy in Cancer Treatment)
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Review

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18 pages, 2480 KiB  
Review
Recent Update and Drug Target in Molecular and Pharmacological Insights into Autophagy Modulation in Cancer Treatment and Future Progress
by Md. Ataur Rahman, Abu Saim Mohammad Saikat, Md. Saidur Rahman, Mobinul Islam, Md. Anowar Khasru Parvez and Bonglee Kim
Cells 2023, 12(3), 458; https://doi.org/10.3390/cells12030458 - 31 Jan 2023
Cited by 12 | Viewed by 3027
Abstract
Recent evidence suggests that autophagy is a governed catabolic framework enabling the recycling of nutrients from injured organelles and other cellular constituents via a lysosomal breakdown. This mechanism has been associated with the development of various pathologic conditions, including cancer and neurological disorders; [...] Read more.
Recent evidence suggests that autophagy is a governed catabolic framework enabling the recycling of nutrients from injured organelles and other cellular constituents via a lysosomal breakdown. This mechanism has been associated with the development of various pathologic conditions, including cancer and neurological disorders; however, recently updated studies have indicated that autophagy plays a dual role in cancer, acting as a cytoprotective or cytotoxic mechanism. Numerous preclinical and clinical investigations have shown that inhibiting autophagy enhances an anticancer medicine’s effectiveness in various malignancies. Autophagy antagonists, including chloroquine and hydroxychloroquine, have previously been authorized in clinical trials, encouraging the development of medication-combination therapies targeting the autophagic processes for cancer. In this review, we provide an update on the recent research examining the anticancer efficacy of combining drugs that activate cytoprotective autophagy with autophagy inhibitors. Additionally, we highlight the difficulties and progress toward using cytoprotective autophagy targeting as a cancer treatment strategy. Importantly, we must enable the use of suitable autophagy inhibitors and coadministration delivery systems in conjunction with anticancer agents. Therefore, this review briefly summarizes the general molecular process behind autophagy and its bifunctional role that is important in cancer suppression and in encouraging tumor growth and resistance to chemotherapy and metastasis regulation. We then emphasize how autophagy and cancer cells interacting with one another is a promising therapeutic target in cancer treatment. Full article
(This article belongs to the Special Issue Molecular Targets for Autophagy in Cancer Treatment)
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18 pages, 1262 KiB  
Review
Autophagy in Cancer Immunotherapy
by Yuhe Lei, Enxin Zhang, Liangliang Bai and Yingjie Li
Cells 2022, 11(19), 2996; https://doi.org/10.3390/cells11192996 - 26 Sep 2022
Cited by 19 | Viewed by 2977
Abstract
Autophagy is a stress-induced process that eliminates damaged organelles and dysfunctional cargos in cytoplasm, including unfolded proteins. Autophagy is involved in constructing the immunosuppressive microenvironment during tumor initiation and progression. It appears to be one of the most common processes involved in cancer [...] Read more.
Autophagy is a stress-induced process that eliminates damaged organelles and dysfunctional cargos in cytoplasm, including unfolded proteins. Autophagy is involved in constructing the immunosuppressive microenvironment during tumor initiation and progression. It appears to be one of the most common processes involved in cancer immunotherapy, playing bidirectional roles in immunotherapy. Accumulating evidence suggests that inducing or inhibiting autophagy contributes to immunotherapy efficacy. Hence, exploring autophagy targets and their modifiers to control autophagy in the tumor microenvironment is an emerging strategy to facilitate cancer immunotherapy. This review summarizes recent studies on the role of autophagy in cancer immunotherapy, as well as the molecular targets of autophagy that could wake up the immune response in the tumor microenvironment, aiming to shed light on its immense potential as a therapeutic target to improve immunotherapy. Full article
(This article belongs to the Special Issue Molecular Targets for Autophagy in Cancer Treatment)
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