Roles of Non-Coding RNAs on Anaplastic Thyroid Carcinomas

Abstract

Anaplastic thyroid cancer (ATC) remains as one of the most aggressive human carcinomas with poor survival rates in patients with the cancer despite therapeutic interventions. Novel targeted and personalized therapies could solve the puzzle of poor survival rates of patients with ATC. In this review, we discuss the role of non-coding RNAs in the regulation of gene expression in ATC as well as how the changes in their expression could potentially reshape the characteristics of ATCs. A broad range of miRNA, such as miR-205, miR-19a, miR-17-3p and miR-17-5p, miR-618, miR-20a, miR-155, etc., have abnormal expressions in ATC tissues and cells when compared to those of non-neoplastic thyroid tissues and cells. Moreover, lncRNAs, such as H19, Human leukocyte antigen (HLA) complex P5 (HCP5), Urothelial carcinoma-associated 1 (UCA1), Nuclear paraspeckle assembly transcript 1 (NEAT1), etc., participate in transcription and post-transcriptional regulation of gene expression in ATC cells. Dysregulations of these non-coding RNAs were associated with development and progression of ATC by modulating the functions of oncogenes during tumour progression. Thus, restoration of the abnormal expression of these miRNAs and lncRNAs may serve as promising ways to treat the patients with ATC. In addition, siRNA mediated inhibition of several oncogenes may act as a potential option against ATC. Thus, non-coding RNAs can be useful as prognostic biomarkers and potential therapeutic targets for the better management of patients with ATC.

Molecular Pathology of Poorly Differentiated and Anaplastic Thyroid Cancer: What Do Pathologists Need to Know?

“…Non-protein-producing RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are potential targets to treat poorly differentiated and anaplastic thyroid carcinoma and likely play an important role in their pathogenesis [ 52 ]. In addition, small interfering RNAs (siRNA) mediate transcriptional gene silencing in cells through DNA methylation and histone modification.…”

“…In anaplastic thyroid carcinoma, several microRNAs are known to be dysregulated [ 52 ]. For instance, the miR-30 family of tumor suppressor microRNAs has been found to be downregulated [ 56 ], and miR-30a overexpression has been shown to suppress migration, tumor spreading, and metastasis in vitro and in vivo [ 57 ].…”

“…Thus, several lncRNA have been shown to be up or downregulated in anaplastic cancer, possessing either tumor suppressive or oncogenic activity. Extensive reviews of lncRNAs regulation in anaplastic carcinomas are available in the recent literature [ 52 , 71 ]. High expression of lncRNA H19 gene has been shown to promote initiation, progression, and therapy resistance of anaplastic carcinoma [ 72 ].…”

Thyroid Carcinoma: Phenotypic Features, Underlying Biology and Potential Relevance for Targeting Therapy

“…Recent findings in miRNA deregulation studies have revealed aberrant miRNA (miR-222, miR-221, and miR-146b) expression increase in PTC tumor tissues in comparison with normal thyroid tissues [ 172 ]. Similarly, miRNAs have been found abnormally expressed in ATC tissues and cells compared with that in non-neoplastic thyroid tissues and cells [ 173 ]. A believed target of these miRNAs was assumed to be c-KIT that functions as a tyrosine kinase receptor and plays a critical role in cell differentiation and growth.…”

Circulating miR-618 Has Prognostic Significance in Patients with Metastatic Colon Cancer

“…Several studies show that dysregulation of miR-618 may play a determinant role in the pathogenesis in a number of solid tumors—breast cancer [ 7 , 8 ], hepatocellular carcinoma [ 9 ], head and neck squamous cell carcinoma [ 10 ], thyroid cancer [ 11 , 12 , 13 ], prostate cancer [ 14 , 15 ], gastric cancer [ 16 , 17 ], bladder cancer [ 18 ], osteosarcoma [ 19 , 20 ] and esophageal adenocarcinoma [ 21 ]—and a hematology malignancy—follicular lymphoma [ 22 ]. This miRNA has been thoroughly investigated in tumor tissue, and yet, little is known regarding its levels of expression in the blood.…”