Kinases and GTPases in Cancer: The Role of Mutations and sRNAs

Topic Information

Dear Colleagues,

Kinases and GTPases are central regulators of cellular signaling, and their dysregulation is a hallmark of cancer. This topic explores two primary mechanisms driving oncogenesis: direct genetic mutations and post-transcriptional modulation by small non-coding RNAs (sRNAs). Activating mutations in GTPases (such as KRAS) or upstream kinases frequently lock these proteins in a constitutively active state, leading to uncontrolled proliferation, survival, and metastasis. Concurrently, sRNAs—including microRNAs (miRNAs) and small interfering RNAs (siRNAs)—play a dual role by either suppressing or promoting tumor progression. These molecules can modulate the expression of kinases and GTPases, creating complex regulatory loops that influence drug resistance and metastatic potential. Understanding the interplay between mutational activation and sRNA-mediated regulation is critical for deciphering cancer heterogeneity. Ultimately, this integrated view highlights novel diagnostic biomarkers and therapeutic opportunities, such as mutant-specific inhibitors or RNA-based strategies aimed at restoring normal signaling network homeostasis.

Dr. Jonas Cicenas
Prof. Dr. Lee M. Graves
Topic Editors

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Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	4.5	7.8	2013	18.2 Days	CHF 2600	Submit
Cancers cancers	4.8	9.0	2009	17.5 Days	CHF 2900	Submit
Cells cells	6.0	11.4	2012	14.9 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	5.6	10.0	2000	17.5 Days	CHF 2900	Submit
Kinases and Phosphatases kinasesphosphatases	-	-	2023	23.8 Days	CHF 1000	Submit
Medicina medicina	2.9	4.6	1920	17.4 Days	CHF 2200	Submit
Sci sci	4.1	5.4	2019	28.2 Days	CHF 1400	Submit

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All Biomedicines Cancers Cells IJMS Kinases and Phosphatases Medicina Sci

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Open AccessEditorial

Mutations of Kinases and GTPases in Cancers

by Jonas Cicenas, Ramojus Balevičius, Rytė Bagdanavičiūtė and Jokūbas Šimkus

Cancers 2026, 18(13), 2033; https://doi.org/10.3390/cancers18132033 - 23 Jun 2026

Viewed by 1082

Abstract

Cancer is a genetic disease driven by the accumulation of mutations that disrupt normal cellular growth. Among the most frequently mutated families are protein kinases, inositol polyphosphate kinases, and GTPases, which together function as central molecular switches controlling proliferation, survival, and metabolism. In [...] Read more.

Cancer is a genetic disease driven by the accumulation of mutations that disrupt normal cellular growth. Among the most frequently mutated families are protein kinases, inositol polyphosphate kinases, and GTPases, which together function as central molecular switches controlling proliferation, survival, and metabolism. In cancer, activating mutations in protein kinases, such as EGFR and BRAF, lead to uncontrolled downstream signaling by locking these enzymes in a constitutively active state. Similarly, mutations affecting inositol kinases, notably PI3KCA, hyperactivate the PI3K/AKT pathway, promoting relentless cell survival and resistance to apoptosis. GTPases, particularly Ras family members (KRAS, NRAS, HRAS), are classical oncogenes where single amino acid substitutions impair their intrinsic GTP hydrolysis activity, trapping them in a persistently GTP-bound “on” state. This unleashes continuous mitogenic signaling independently of external growth factors. Collectively, these mutations are not random but converge on a limited set of core pathways, making them key drivers of tumor initiation and progression. Understanding the specific molecular consequences of kinase and GTPase mutations has directly informed the development of targeted therapies, including small molecule inhibitors and monoclonal antibodies, now used in routine clinical practice. Full article

(This article belongs to the Topic Kinases and GTPases in Cancer: The Role of Mutations and sRNAs)

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