GTPases in Cancers: Therapeutic Opportunities and Challenges

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

Deadline for manuscript submissions: 31 December 2024 | Viewed by 762

Special Issue Editors


E-Mail Website
Guest Editor
University of Rochester Medical Center, Rochester, NY, USA
Interests: cancer biology; small molecule; inflammation; immunity; drug

E-Mail Website
Guest Editor
University of Rochester Medical Center, Rochester, NY, USA
Interests: medicinal chemistry; cancer biology; tumor immunology

Special Issue Information

Dear Colleagues,

GTPases are critical molecular switches in cell functions. GTPases play crucial roles in multiple cellular physiological processes, such as cell signaling, cell cycle regulation, and maintenance of cell polarity. Their abnormal activation or inactivation is closely associated with the occurrence and development of various diseases. Currently, GTPases are being investigated for their roles in malignancies, neurodegenerative diseases and cardiomyopathies. GTPases are considered difficult to target.

However, with the recent approval of KRAS inhibitors for treating pancreatic cancer and other high-risk malignancies, there is a renewed importance in re-examining GTPases to define their roles in diverse cancer states and to develop novel therapeutic agents. This re-evaluation is expected to unveil specific functions of GTPases in various cancer types, providing a foundation for designing more effective treatment strategies and opening up new avenues for developing innovative treatment targets and drugs. Since the recent approval of KRAS inhibitors for the treatment of pancreatic and other higher risk malignancies, GTPases deserve a revisit to define their roles in diverse disease states and novel develop therapeutic agents.

In this Special Issue, original research articles and reviews are welcome. We look forward to receiving your contributions. 

Dr. Rakesh K. K. Singh
Dr. Kyu Kwang Kim
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. 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

  • GTAPses
  • cancer
  • Alzheimer’s disease
  • pulmonary diseases
  • cardiovascular diseases
  • cell cycle
  • proliferation
  • secretion machinery and proteins

Published Papers (1 paper)

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Research

16 pages, 3492 KiB  
Article
Forchlorfenuron-Induced Mitochondrial Respiration Inhibition and Metabolic Shifts in Endometrial Cancer
by Kyukwang Kim, Negar Khazan, Rachael B. Rowswell-Turner, Rakesh K. Singh, Taylor Moore, Myla S. Strawderman, John P. Miller, Cameron W. A. Snyder, Ahmad Awada and Richard G. Moore
Cancers 2024, 16(5), 976; https://doi.org/10.3390/cancers16050976 - 28 Feb 2024
Viewed by 644
Abstract
Forchlorfenuron (FCF) is a widely used plant cytokinin that enhances fruit quality and size in agriculture. It also serves as a crucial pharmacological tool for the inhibition of septins. However, the precise target of FCF has not yet been fully determined. This study [...] Read more.
Forchlorfenuron (FCF) is a widely used plant cytokinin that enhances fruit quality and size in agriculture. It also serves as a crucial pharmacological tool for the inhibition of septins. However, the precise target of FCF has not yet been fully determined. This study reveals a novel target of FCF and elucidates its downstream signaling events. FCF significantly impairs mitochondrial respiration and mediates metabolic shift toward glycolysis, thus making cells more vulnerable to glycolysis inhibition. Interestingly, FCF’s impact on mitochondrial function persists, even in cells lacking septins. Furthermore, the impaired mitochondrial function leads to the degradation of HIF-1α, facilitated by increased cellular oxygen. FCF also induces AMPK activation, suppresses Erk1/2 phosphorylation, and reduces the expression of HER2, β-catenin, and PD-L1. Endometrial cancer is characterized by metabolic disorders such as diabetes and aberrant HER2/Ras-Erk1/2/β-catenin signaling. Thus, FCF may hold promise as a potential therapeutic in endometrial cancer. Full article
(This article belongs to the Special Issue GTPases in Cancers: Therapeutic Opportunities and Challenges)
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