Small GTPases in Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 January 2016) | Viewed by 44305

Special Issue Editor


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Guest Editor
1. Proteomics Center, Institute of Biochemistry, Vilnius University Life Sciences Center, Sauletekio al. 7, LT-10257 Vilnius, Lithuania
2. MAP Kinase Resource, Bioinformatics, Melchiorstrasse 9, CH-3027 Bern, Switzerland
Interests: breast cancer; prostate cancer; acute myeloid leukemia (AML); kinases
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Dear Colleagues,

The Ras superfamily of GTPases comprises several subfamilies of small GTP-binding proteins whose functions have been implicated in the control of cell proliferation, differentiation, protein transport, cytoskeleton organization, etc. Ras proteins are key components of the signal transduction pathways triggered by a number of different extracellular signals, such as mitogens. KRAS and NRAS mutations have been implicated in quite a number of human cancers. Deregulation of many upstream molecules also triggers deregulation of the activity of Ras proteins, leading to the development of cancer. Rho GTPases are involved in multiple cellular processes that could also affect cancer progression, namely cytoskeletal organization, cell cycle progression, the regulation of transcription, and protein trafficking. Some Rho GTPases have been shown to have oncogenic activity and/or can promote cancer cell invasion. Con the other hand, as other subfamily members, appear to act as tumor suppressors and are deleted, mutated or deregulated in some cancers. Rab subfamily members are mostly involved in vesicular trafficking and it seems that deregulation of some of them is correlated with a worsened outcome in human cancers. In this Special Issue of Cancers, "Small GTPases in Cancer", experts are invited to contribute original research papers or review articles that will provide further insights on the various functions of small GTPases in cancers, their role in cancer biology, as well as a possibility to use them as drug targets and biomarkers.

Dr. Jonas Cicenas
Guest Editor

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Keywords

  • small GTPases
  • Ras family
  • Ras
  • Rab
  • Rho
  • KRAS mutations
  • NRAS mutations
  • cancer
  • biomarkers

Published Papers (3 papers)

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Review

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Review
KRAS, TP53, CDKN2A, SMAD4, BRCA1, and BRCA2 Mutations in Pancreatic Cancer
by Jonas Cicenas, Kotryna Kvederaviciute, Ingrida Meskinyte, Edita Meskinyte-Kausiliene, Aiste Skeberdyte and Jonas Cicenas
Cancers 2017, 9(5), 42; https://doi.org/10.3390/cancers9050042 - 28 Apr 2017
Cited by 183 | Viewed by 13865
Abstract
Pancreatic cancer is a disease that has a very high fatality rate and one of the highest mortality ratios among all major cancers, remaining the fourth leading cause of cancer-related deaths in developed countries. The major treatment of pancreatic cancer is surgery; however, [...] Read more.
Pancreatic cancer is a disease that has a very high fatality rate and one of the highest mortality ratios among all major cancers, remaining the fourth leading cause of cancer-related deaths in developed countries. The major treatment of pancreatic cancer is surgery; however, only 15–20% of patients are candidates for it at the diagnosis of disease. On the other hand, survival in patients, who undergo surgery, is less than 30%. In most cancers, genome stability is disturbed and pancreatic cancer is not the exception. Approximately 97% of pancreatic cancers have gene derangements, defined by point mutations, amplifications, deletions, translocations, and inversions. This review describes the most frequent genetic alterations found in pancreatic cancer. Full article
(This article belongs to the Special Issue Small GTPases in Cancer)
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1518 KiB  
Review
KRAS Mutant Pancreatic Cancer: No Lone Path to an Effective Treatment
by Daniel Zeitouni, Yuliya Pylayeva-Gupta, Channing J. Der and Kirsten L. Bryant
Cancers 2016, 8(4), 45; https://doi.org/10.3390/cancers8040045 - 18 Apr 2016
Cited by 135 | Viewed by 19115
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest cancers with a dismal 7% 5-year survival rate and is projected to become the second leading cause of cancer-related deaths by 2020. KRAS is mutated in 95% of PDACs and is a well-validated driver of [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest cancers with a dismal 7% 5-year survival rate and is projected to become the second leading cause of cancer-related deaths by 2020. KRAS is mutated in 95% of PDACs and is a well-validated driver of PDAC growth and maintenance. However, despite comprehensive efforts, an effective anti-RAS drug has yet to reach the clinic. Different paths to inhibiting RAS signaling are currently under investigation in the hope of finding a successful treatment. Recently, direct RAS binding molecules have been discovered, challenging the perception that RAS is an “undruggable” protein. Other strategies currently being pursued take an indirect approach, targeting proteins that facilitate RAS membrane association or downstream effector signaling. Unbiased genetic screens have identified synthetic lethal interactors of mutant RAS. Most recently, metabolic targets in pathways related to glycolytic signaling, glutamine utilization, autophagy, and macropinocytosis are also being explored. Harnessing the patient’s immune system to fight their cancer is an additional exciting route that is being considered. The “best” path to inhibiting KRAS has yet to be determined, with each having promise as well as potential pitfalls. We will summarize the state-of-the-art for each direction, focusing on efforts directed toward the development of therapeutics for pancreatic cancer patients with mutated KRAS. Full article
(This article belongs to the Special Issue Small GTPases in Cancer)
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1663 KiB  
Review
Mechanisms of Nuclear Export in Cancer and Resistance to Chemotherapy
by Mohamed El-Tanani, El-Habib Dakir, Bethany Raynor and Richard Morgan
Cancers 2016, 8(3), 35; https://doi.org/10.3390/cancers8030035 - 14 Mar 2016
Cited by 33 | Viewed by 10580
Abstract
Tumour suppressor proteins, such as p53, BRCA1, and ABC, play key roles in preventing the development of a malignant phenotype, but those that function as transcriptional regulators need to enter the nucleus in order to function. The export of proteins between the nucleus [...] Read more.
Tumour suppressor proteins, such as p53, BRCA1, and ABC, play key roles in preventing the development of a malignant phenotype, but those that function as transcriptional regulators need to enter the nucleus in order to function. The export of proteins between the nucleus and cytoplasm is complex. It occurs through nuclear pores and exported proteins need a nuclear export signal (NES) to bind to nuclear exportin proteins, including CRM1 (Chromosomal Region Maintenance protein 1), and the energy for this process is provided by the RanGTP/RanGDP gradient. Due to the loss of DNA repair and cell cycle checkpoints, drug resistance is a major problem in cancer treatment, and often an initially successful treatment will fail due to the development of resistance. An important mechanism underlying resistance is nuclear export, and a number of strategies that can prevent nuclear export may reverse resistance. Examples include inhibitors of CRM1, antibodies to the nuclear export signal, and alteration of nuclear pore structure. Each of these are considered in this review. Full article
(This article belongs to the Special Issue Small GTPases in Cancer)
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