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NF-κB in Thyroid Cancer: An Update
Elvira Crescenzi1, Antonio Leonardi2, Francesco Pacifico1
1Istituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (CNR), Via S. Pansini, 5, 80131 Naples, Italy.
Abstract:
The dysregulated NF-κB basal activity is a common feature of human thyroid carcinomas, especially in poorly differentiated or undifferentiated forms that, even if rare, are often resistant to standard therapies, and, therefore, are uncurable. Despite the molecular mechanisms leading to NF-κB activation in thyroid cancer being only partially understood, during the last few years, it has become clear that NF-κB contributes in different ways to the oncogenic potential of thyroid neoplastic cells. Indeed, it enhances their proliferation and viability, promotes their migration to and colonization of distant organs, and fuels their microenvironment. In addition, NF-κB signaling plays an important role in cancer stem cells from more aggressive thyroid carcinomas. Interfering with the different upstream and/or downstream pathways that drive NF-κB activity in thyroid neoplastic cells is an attractive strategy for the development of novel therapeutic drugs capable of overcoming the therapy resistance of advanced thyroid carcinomas. This review focuses on the recent findings about the key functions of NF-κB in thyroid cancer and discusses the potential implications of targeting NF-κB in advanced thyroid carcinomas.
Insights
Dysregulated nuclear factor-kappa B (NF-κB) activity drives thyroid cancer progression and therapy resistance. Targeting NF-κB pathways offers a promising strategy for treating advanced, aggressive thyroid carcinomas.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Nuclear factor-kappa B (NF-κB) dysregulation is prevalent in human thyroid carcinomas, particularly in aggressive, poorly differentiated, and undifferentiated subtypes.
- These advanced thyroid cancers often exhibit resistance to conventional therapies, leading to poor prognoses.
Purpose of the Study:
- To review recent findings on the critical roles of NF-κB in thyroid cancer pathogenesis.
- To explore the therapeutic potential of targeting NF-κB signaling in advanced thyroid carcinomas.
Main Methods:
- Literature review of recent studies on NF-κB signaling in thyroid cancer.
- Analysis of NF-κB's contribution to cancer cell proliferation, survival, migration, and microenvironment modulation.
- Examination of NF-κB's role in thyroid cancer stem cells.
Main Results:
- NF-κB enhances thyroid cancer cell proliferation, viability, and migration.
- NF-κB signaling fuels the tumor microenvironment and is crucial in cancer stem cells of aggressive thyroid carcinomas.
- While mechanisms are partially understood, NF-κB activation significantly contributes to thyroid cancer's oncogenic potential.
Conclusions:
- Targeting upstream or downstream NF-κB pathways presents a viable strategy for developing novel therapeutics.
- Interfering with NF-κB signaling may overcome therapy resistance in advanced thyroid carcinomas.
- NF-κB represents a key therapeutic target for improving outcomes in aggressive thyroid cancer.
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