RMRP, RMST, FTX and IPW: novel potential long non-coding RNAs in medullary thyroid cancer.
Berta Luzón-ToroLeticia Villalba-BenitoRaquel María FernándezAna TorroglosaGuillermo AntiñoloSalud BorregoPublished in: Orphanet journal of rare diseases (2021)
The relevant role of long non-coding RNAs (lncRNAs) in cancer is currently a matter of increasing interest. Medullary thyroid cancer (MTC) is a rare neuroendocrine tumor (2-5% of all thyroid cancer) derived from the parafollicular C-cells which secrete calcitonin. About 75% of all medullary thyroid cancers are believed to be sporadic medullary thyroid cancer (sMTC), whereas the remaining 25% correspond to inherited cancer syndromes known as Multiple Endocrine Neoplasia type 2 (MEN2). MEN2 syndrome, with autosomal dominant inheritance is caused by germline gain of function mutations in RET proto-oncogene. To date no lncRNA has been associated to MEN2 syndrome and only two articles have been published relating long non-coding RNA (lncRNA) to MTC: the first one linked MALAT1 with sMTC and, in the other, our group determined some new lncRNAs in a small group of sMTC cases in fresh tissue (RMST, FTX, IPW, PRNCR1, ADAMTS9-AS2 and RMRP). The aim of the current study is to validate such novel lncRNAs previously described by our group by using a larger cohort of patients, in order to discern their potential role in the disease. Here we have tested three up-regulated (RMST, FTX, IPW) and one down-regulated (RMRP) lncRNAs in our samples (formalin fixed paraffin embedded tissues from twenty-one MEN2 and ten sMTC patients) by RT-qPCR analysis. The preliminary results reinforce the potential role of RMST, FTX, IPW and RMRP in the pathogenesis of MTC.
Keyphrases
- long non coding rna
- poor prognosis
- newly diagnosed
- ejection fraction
- prognostic factors
- network analysis
- transcription factor
- papillary thyroid
- gene expression
- induced apoptosis
- chronic kidney disease
- human health
- climate change
- oxidative stress
- patient reported outcomes
- risk assessment
- dna repair
- childhood cancer
- patient reported
- cell proliferation
- copy number
- dna damage