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Published on: February 16, 2017
AKT: A Central Node in Complex Signaling Cascades
Kentaro Minegishi1, Yoh Dobashi2, Emi Kimura2
1Department of Thoracic Surgery, Jichi Medical University, 330-8503 Saitama, Saitama, Japan.
Abstract:
Akt (v-akt murine thymoma virus oncogene homologue) is a well-known serine-threonine kinase that functions as a central node in various important signal cascades involved in cellular maintenance. Akt has also been implicated in oncogenic malignancies as evidenced by protein overexpression, activation and somatic aberration of components in the phosphoinositide-3 kinase-Akt pathway. As such, Akt is a potential target in cancer therapy. Akt is frequently activated in human cancer tissues not only due to aberrant upstream signaling, but also by genetic mutations in AKT itself. This leads to the aberrant activation of pathways downstream of Akt that regulate cell-cycle progression and metabolism as well as activation of transcription factors that promote oncogenesis. In this review, we summarize previous research on Akt, including the molecular mechanisms underlying Akt signal transduction, as well as its physiologic roles and the pathologic consequences when dysregulated. We also discuss the roles of dysregulated protein overexpression/activation, increases in gene copy number, single nucleotide polymorphisms and the network of non-coding RNAs that regulate this pathway, with a particular focus on lung carcinomas. Finally, we discuss strategies that might lead to more effective targeting of Akt for clinical cancer therapy.
Insights
The Akt signaling pathway is crucial for cell maintenance but its dysregulation, through mutations or overexpression, drives cancer. Targeting Akt offers a promising strategy for effective cancer therapy.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- The Akt (v-akt murine thymoma virus oncogene homologue) kinase is central to cellular maintenance and signal transduction.
- Aberrant activation of the phosphoinositide-3 kinase-Akt pathway, via overexpression or mutation, is implicated in oncogenic malignancies.
Purpose of the Study:
- To review the molecular mechanisms of Akt signal transduction.
- To discuss the physiological roles and pathological consequences of Akt dysregulation in cancer.
- To explore therapeutic strategies targeting Akt, particularly in lung carcinomas.
Main Methods:
- Literature review of existing research on Akt signaling.
- Analysis of genetic and non-coding RNA regulatory mechanisms.
- Focus on Akt's role in human cancer tissues, especially lung carcinomas.
Main Results:
- Akt is frequently activated in human cancers due to upstream signaling issues or intrinsic AKT gene mutations.
- Dysregulated Akt signaling impacts cell-cycle progression, metabolism, and transcription factor activation, promoting oncogenesis.
- Non-coding RNAs also play a regulatory role in the Akt pathway.
Conclusions:
- Akt is a significant therapeutic target in cancer due to its central role in oncogenesis.
- Understanding the multifaceted regulation of Akt is key to developing effective cancer therapies.
- Targeting Akt pathways, considering genetic alterations and regulatory networks, holds promise for clinical applications.
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