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mTOR Signaling in Anti-cancer Therapy Research
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mTOR Signaling in Anti-cancer Therapy Research

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 (20 October 2024) | Viewed by 3789

Special Issue Editor

Prof. Dr. Ji-Youn Jung

E-Mail Website
Guest Editor
Department of Companion and Laboratory Animal Science, Kongju National University, Daehak-ro, Yesan-gun, Gongju-si 32439, Chungcheongnam-do , Republic of Korea
Interests: anti-cancer; autophagy; apoptosis; flavonoids

Special Issue Information

Dear Colleagues,

The mechanistic target of the rapamycin (mTOR) pathway is the main signaling cascade activated in various cancer cells, and its activation can promote carcinogenesis. The mTOR signaling pathway not only regulates gene transcription and protein synthesis to regulate cell proliferation and immune cell differentiation but also plays an important role in cancer metabolism. The mTOR pathway is potentially associated with apoptosis and autophagy and plays a key role in cancer. As a result, the mTOR signaling pathway is a popular target in anti-cancer therapy research.

This Special Issue concentrates on the role of the mTOR signaling pathway in anti-cancer therapy research. The papers published here will certainly contribute to the ever-growing cancer research and provide a new insight into the anti-cancer mechanism.

Prof. Dr. Ji-Youn Jung
Guest Editor

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. 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

  • mTOR
  • cancer
  • apoptosis
  • autophagy
  • cancer metabolism

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Published Papers (2 papers)

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Research

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17 pages, 2873 KiB  
Article
Assembly of mTORC3 Involves Binding of ETV7 to Two Separate Sequences in the mTOR Kinase Domain
by Jun Zhan, Frank Harwood, Sara Ten Have, Angus Lamond, Aaron H. Phillips, Richard W. Kriwacki, Priyanka Halder, Monica Cardone and Gerard C. Grosveld
Int. J. Mol. Sci. 2024, 25(18), 10042; https://doi.org/10.3390/ijms251810042 - 18 Sep 2024
Cited by 1 | Viewed by 1158
Abstract
mTOR plays a crucial role in cell growth by controlling ribosome biogenesis, metabolism, autophagy, mRNA translation, and cytoskeleton organization. It is a serine/threonine kinase that is part of two distinct extensively described protein complexes, mTORC1 and mTORC2. We have identified a rapamycin-resistant mTOR [...] Read more.
mTOR plays a crucial role in cell growth by controlling ribosome biogenesis, metabolism, autophagy, mRNA translation, and cytoskeleton organization. It is a serine/threonine kinase that is part of two distinct extensively described protein complexes, mTORC1 and mTORC2. We have identified a rapamycin-resistant mTOR complex, called mTORC3, which is different from the canonical mTORC1 and mTORC2 complexes in that it does not contain the Raptor, Rictor, or mLST8 mTORC1/2 components. mTORC3 phosphorylates mTORC1 and mTORC2 targets and contains the ETS transcription factor ETV7, which binds to mTOR and is essential for mTORC3 assembly in the cytoplasm. Tumor cells that assemble mTORC3 have a proliferative advantage and become resistant to rapamycin, indicating that inhibiting mTORC3 may have a therapeutic impact on cancer. Here, we investigate which domains or amino acid residues of ETV7 and mTOR are involved in their mutual binding. We found that the mTOR FRB and LBE sequences in the kinase domain interact with the pointed (PNT) and ETS domains of ETV7, respectively. We also found that forced expression of the mTOR FRB domain in the mTORC3-expressing, rapamycin-resistant cell line Karpas-299 out-competes mTOR for ETV7 binding and renders these cells rapamycin-sensitive in vivo. Our data provide useful information for the development of molecules that prevent the assembly of mTORC3, which may have therapeutic value in the treatment of mTORC3-positive cancer. Full article
(This article belongs to the Special Issue mTOR Signaling in Anti-cancer Therapy Research)
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Review

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17 pages, 5932 KiB  
Review
Interplay between mTOR and Purine Metabolism Enzymes and Its Relevant Role in Cancer
by Simone Allegrini, Marcella Camici, Mercedes Garcia-Gil, Rossana Pesi and Maria Grazia Tozzi
Int. J. Mol. Sci. 2024, 25(12), 6735; https://doi.org/10.3390/ijms25126735 - 19 Jun 2024
Cited by 6 | Viewed by 2049
Abstract
Tumor cells reprogram their metabolism to meet the increased demand for nucleotides and other molecules necessary for growth and proliferation. In fact, cancer cells are characterized by an increased “de novo” synthesis of purine nucleotides. Therefore, it is not surprising that specific enzymes [...] Read more.
Tumor cells reprogram their metabolism to meet the increased demand for nucleotides and other molecules necessary for growth and proliferation. In fact, cancer cells are characterized by an increased “de novo” synthesis of purine nucleotides. Therefore, it is not surprising that specific enzymes of purine metabolism are the targets of drugs as antineoplastic agents, and a better knowledge of the mechanisms underlying their regulation would be of great help in finding new therapeutic approaches. The mammalian target of the rapamycin (mTOR) signaling pathway, which is often activated in cancer cells, promotes anabolic processes and is a major regulator of cell growth and division. Among the numerous effects exerted by mTOR, noteworthy is its empowerment of the “de novo” synthesis of nucleotides, accomplished by supporting the formation of purinosomes, and by increasing the availability of necessary precursors, such as one-carbon formyl group, bicarbonate and 5-phosphoribosyl-1-pyrophosphate. In this review, we highlight the connection between purine and mitochondrial metabolism, and the bidirectional relation between mTOR signaling and purine synthesis pathways. Full article
(This article belongs to the Special Issue mTOR Signaling in Anti-cancer Therapy Research)
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