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Transient oncogenes
1Department of Biophysics and Center of Biotechnology, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Brazil. lenz@ufrgs.br
Abstract:
A given cancer is produced by a unique combination of genetic alterations that target specific genes, most often leading to activation of oncogenes and inactivation of tumor suppressor genes. Traditional oncogenes, such as RasV12, are involved in maintaining pro-survival and proliferation signals activated in the cell. Several evidences suggest that cancer cells are addicted to oncogenes and that their inhibition has dramatic effects on cancer cells. Here, the hypothesis that oncogenes may be activated only transiently and that this short activation may be important for cancer formation by affecting the differentiation state of the cancer cells is presented. These "transient oncogenes" are overlooked in genomic or proteomic analysis due to their transient nature. Here we argue that transcription factors, such as the so called Yamanaka factors, capable of reprogramming cells to a less differentiated state, which normally happens to cancer cells, can function as transient oncogenes. Several published evidences are used to support the proposed hypothesis. Analysis and even targeting of this new class of oncogenes could have a great impact on cancer biology, treatment and, most importantly, prevention.
Insights
Cancer cells may rely on transient oncogenes, like Yamanaka factors, for formation by altering cell differentiation. Targeting these overlooked factors could revolutionize cancer treatment and prevention.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cancer arises from genetic alterations activating oncogenes and inactivating tumor suppressor genes.
- Cancer cells exhibit addiction to oncogenes, making their inhibition a therapeutic strategy.
- Traditional oncogenes (e.g., RasV12) sustain pro-survival and proliferation signals.
Purpose of the Study:
- To propose the hypothesis that oncogenes can be transiently activated.
- To investigate the role of transient oncogene activation in cancer formation by affecting cell differentiation.
- To highlight the potential of "transient oncogenes" as a new class of targets in cancer research.
Main Methods:
- Review and synthesis of published evidence supporting the transient oncogene hypothesis.
- Analysis of transcription factors, such as Yamanaka factors, as potential transient oncogenes.
- Discussion of the implications for genomic and proteomic analyses.
Main Results:
- Transient oncogene activation, particularly by factors influencing cell differentiation, is proposed as crucial for cancer development.
- Yamanaka factors are suggested as candidates for transient oncogenes due to their cell-reprogramming capabilities.
- Transient oncogenes are likely missed in standard genomic/proteomic analyses due to their short-lived nature.
Conclusions:
- Transient oncogenes represent a novel class of oncogenic drivers potentially critical in cancer biology.
- Identifying and targeting these transient factors could offer new avenues for cancer treatment and prevention.
- Further research into transient oncogenes may significantly impact our understanding and management of cancer.
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