Journal
CANCER SCIENCE
Volume 111, Issue 8, Pages 2672-2681Publisher
WILEY
DOI: 10.1111/cas.14509
Keywords
non-coding RNA; signal transduction; Smad; transcription; transforming growth factor-beta
Categories
Funding
- Cancerfonden [CAN 2018/469]
- Vetenskapsradet [2018-02757]
- Ludwig Institute for Cancer Research
- Barncancerfonden [2018-0091]
- Swedish Research Council [2018-02757] Funding Source: Swedish Research Council
- Vinnova [2018-02757] Funding Source: Vinnova
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Cancer is driven by genetic mutations in oncogenes and tumor suppressor genes and by cellular events that develop a misregulated molecular microenvironment in the growing tumor tissue. The tumor microenvironment is guided by the excessive action of specific cytokines including transforming growth factor-beta (TGF-beta), which normally controls embryonic development and the homeostasis of young or adult tissues. As a consequence of the genetic alterations generating a given tumor, TGF-beta can preserve its homeostatic function and attempt to limit neoplastic expansion, whereas, once the tumor has progressed to an aggressive stage, TGF-beta can synergize with various oncogenic stimuli to facilitate tumor invasiveness and metastasis. TGF-beta signaling mechanisms via Smad proteins, various ubiquitin ligases, and protein kinases are relatively well understood. Such mechanisms regulate the expression of genes encoding proteins or non-coding RNAs. Among non-coding RNAs, much has been understood regarding the regulation and function of microRNAs, whereas the role of long non-coding RNAs is still emerging. This article emphasizes TGF-beta signaling mechanisms leading to the regulation of non-coding genes, the function of such non-coding RNAs as regulators of TGF-beta signaling, and the contribution of these mechanisms in specific hallmarks of cancer.
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