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Cancers
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Targeting the PI3K/AKT/mTOR Pathway in Cancer: Mechanisms and Advances in...
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Targeting the PI3K/AKT/mTOR Pathway in Cancer: Mechanisms and Advances in Clinical Trials

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Biomarkers".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 5233

Special Issue Editors

Dr. Elaine Dunlop

E-Mail Website
Guest Editor
Division of Cancer and Genetics, Cardiff University, Cardiff, UK
Interests: mTOR; tuberous sclerosis complex; autophagy; cancer; cell signalling; tumour microenvironment; extracellular vesicles
Dr. Harilaos Filippakis

E-Mail Website
Guest Editor
Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME, USA
Interests: cancer metabolism; macropinocytosis; lysosome biology; autophagy; mTOR signaling; TSC; LAM

Special Issue Information

Dear Colleagues,

The PI3K/AKT/mTOR signaling pathway is critically important for the regulation of cell growth. Its disruption is seen in many cancer types as well as in a number of inherited syndromes. Our understanding of the multi-layered regulation of this pathway has progressed hugely over the last three decades. This knowledge has improved our understanding of this signaling cascade in both normal physiology and in cancer progression. Targeting the pathway has long been seen as an attractive therapeutic option in oncology and work is ongoing to optimize how inhibiting this pathway can bring the most benefit to cancer patients.

We are pleased to invite you to contribute to a Special Issue on “Targeting the PI3K/AKT/mTOR pathway in Cancer: Mechanisms and Advances in Clinical Trials”. Through this, we hope to highlight the progress the field has made at a molecular level and how this knowledge has been translated to provide new treatment options for the management of cancer patients. We also aim to clarify the gaps in knowledge and challenges that still remain to be addressed.

In this Special Issue, both original research articles and reviews are welcome. Submissions can cover any relevant topic, including PI3K/AKT/mTOR signaling mechanisms, inputs, and feedback; dysregulation of PI3K/AKT/mTOR in cancer; progress in clinical trials; challenges for the field; the future of mTOR-targeted therapeutics.

We look forward to receiving your contributions.

Dr. Elaine Dunlop
Dr. Harilaos Filippakis
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 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

  • PI3K
  • AKT
  • mTOR
  • cancer
  • inhibitor
  • clinical trial
  • oncology

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Published Papers (2 papers)

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Research

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20 pages, 4385 KiB  
Article
FAM107A Inactivation Associated with Promoter Methylation Affects Prostate Cancer Progression through the FAK/PI3K/AKT Pathway
by Shuai Ke, Zelin Liu, Qinghua Wang, Guanzhong Zhai, Haoren Shao, Xi Yu and Jia Guo
Cancers 2022, 14(16), 3915; https://doi.org/10.3390/cancers14163915 - 13 Aug 2022
Cited by 12 | Viewed by 2166
Abstract
Prostate cancer (PCa) is one of the most common cancers and is the second leading cause of mortality in men. Studies exploring novel therapeutic methods are urgently needed. FAM107A, a coding gene located in the short arm of chromosome3, is generally downregulated in [...] Read more.
Prostate cancer (PCa) is one of the most common cancers and is the second leading cause of mortality in men. Studies exploring novel therapeutic methods are urgently needed. FAM107A, a coding gene located in the short arm of chromosome3, is generally downregulated in PCa and is associated with a poor prognosis. However, the downregulation of FAM107A in PCa and the mechanism of its action remain challenging to determine. This investigation found that downregulation of FAM107A expression in PCa was caused by hypermethylation of CpG islands. Furthermore, DNA methyltransferase 1 (DNMT1) was involved in maintaining hypermethylation. Mechanistically, overexpression of FAM107A inhibits tumor cell proliferation, migration, invasion and promotes apoptosis through the FAK/PI3K/AKT signaling pathway, indicating that FAM107A may be a molecular brake of FAK/PI3K/AKT signaling, thus limiting the active state of the FAK/PI3K/AKT pathway. These findings will contribute to a better understanding of the effect of FAM107A in PCa, and FAM107A may represent a new therapeutic target for PCa. Full article
(This article belongs to the Special Issue Targeting the PI3K/AKT/mTOR Pathway in Cancer: Mechanisms and Advances in Clinical Trials)
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Review

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12 pages, 914 KiB  
Review
Targeting mTORC1 Activity to Improve Efficacy of Radioligand Therapy in Cancer
by Michal Grzmil, Fabius Wiesmann, Roger Schibli and Martin Behe
Cancers 2023, 15(1), 17; https://doi.org/10.3390/cancers15010017 - 20 Dec 2022
Cited by 1 | Viewed by 2402
Abstract
Radioligand therapy (RLT) represents an effective strategy to treat malignancy by cancer-selective delivery of radioactivity following systemic application. Despite recent therapeutic successes, cancer radioresistance and insufficient delivery of the radioactive ligands, as well as cytotoxicity to healthy organs, significantly impairs clinical efficacy. To [...] Read more.
Radioligand therapy (RLT) represents an effective strategy to treat malignancy by cancer-selective delivery of radioactivity following systemic application. Despite recent therapeutic successes, cancer radioresistance and insufficient delivery of the radioactive ligands, as well as cytotoxicity to healthy organs, significantly impairs clinical efficacy. To improve disease management while minimizing toxicity, in recent years, the combination of RLT with molecular targeted therapies against cancer signaling networks showed encouraging outcomes. Characterization of the key deregulated oncogenic signaling pathways revealed their convergence to activate the mammalian target of rapamycin (mTOR), in which signaling plays an essential role in the regulation of cancer growth and survival. Therapeutic interference with hyperactivated mTOR pathways was extensively studied and led to the development of mTOR inhibitors for clinical applications. In this review, we outline the regulation and oncogenic role of mTOR signaling, as well as recapitulate and discuss mTOR complex 1 (mTORC1) inhibition to improve the efficacy of RLT in cancer. Full article
(This article belongs to the Special Issue Targeting the PI3K/AKT/mTOR Pathway in Cancer: Mechanisms and Advances in Clinical Trials)
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