LONG NON-CODING RNAS AT THE INTERFACE OF EPIGENETICS AND HORMONAL SIGNALING IN THYROID CANCER
Abstract
Thyroid cancer has emerged as the most common endocrine malignancy and the fifth most frequent cancer among women globally. Rates have roughly doubled compared to previous decades. Hormonal signaling plays a major role in this rise, with receptors for thyroid hormone, estrogen, progesterone, and HER2 activating pathways such as MAPK and PI3K/AKT that drive tumor cells toward proliferation and invasion. Increasingly, research points to long non-coding RNAs (lncRNAs) as the link between these hormone-driven signals and the epigenetic changes occurring inside the cell. Acting as scaffolds, guides, or decoys, lncRNAs shape chromatin structure, DNA methylation, and histone modification in ways that switch tumor suppressor genes off or oncogenes on. Molecules such as HOTAIR, NEAT1, ANRIL, GAS5, CASC2, and MALAT1 have been associated with tumor aggressiveness. Because these RNAs are stable and can be picked up in tissue or body fluids, they're gaining attraction as diagnostic and prognostic markers, which matters given how often fine-needle aspiration biopsies come back inconclusive. The convergence of lncRNA-driven epigenetic regulation and hormonal signaling thus emerges as a central feature of thyroid cancer biology, one with meaningful implications for future biomarkers and treatment strategies.
Keywords
- Thyroid cancer, Epigenetics, long non-coding RNAs (lncRNAs), Hormonal signaling, Thyroid hormones, Biomarkers.
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