<p>Thyroid cancer (TC) represents the most common endocrine malignancy; however, the intricacies of its carcinogenesis pose significant challenges to therapeutic interventions. A comprehensive understanding of the molecular mechanisms that drive TC progression is crucial for the development of effective treatment strategies, especially considering the increasingly recognized role of non-coding RNAs (ncRNAs) in oncogenesis. Notwithstanding recent advancements, the regulatory functions of long non-coding RNAs (lncRNAs) and their interactions with microRNAs (miRNAs) in the context of TC are not yet fully elucidated. This review aims to address this knowledge deficiency by investigating the dual roles of lncRNAs in the pathogenesis of TC, specifically their regulation of programmed cell death (PCD) pathways. Current literature indicates that disrupted competitive endogenous RNA (ceRNA) networks are involved in drug resistance, epithelial–mesenchymal transition (EMT), as well as tumor proliferation, angiogenesis, invasion, and metastasis in TC. The basis of cancer therapy-induced tumor cell elimination is programmed cell death (PCD), which includes well-studied processes such as apoptosis, autophagy, and ferroptosis as well as novel pathways, such as cuproptosis, immunogenic cell death (ICD), and PANoptosis. Recent research has shown the critical function of long non-coding RNAs (lncRNAs) in modifying these several PCD pathways, impacting TC&#xa0;growth and therapy response. This review synthesizes evidence on how lncRNAs regulate PCD to influence TC progression and therapeutic outcomes. Additionally, we examine the clinical relevance of lncRNAs in TC, highlighting their potential as biomarkers for diagnosis and prognosis, therapeutic targets, and contributors to drug resistance, while emphasizing recent advancements in this field.</p>