Original Article
Uncovering the potential miRNAs and mRNAs in follicular variant of papillary thyroid carcinoma in the Cancer Genome Atlas database
Abstract
Background: Understanding the molecule mechanism is a key step in the development of diagnostic and therapeutic measures of follicular variant of papillary thyroid carcinoma. The objective of this study is to identify differentially expressed miRNAs and mRNAs, shedding light on the molecule mechanism of follicular variant of papillary thyroid carcinoma.
Methods: The data of miRNA, mRNA and DNA methylation were downloaded from The Cancer Genome Atlas (TCGA) database. Differential analysis between the follicular variant of papillary thyroid carcinoma and controls was performed in terms of miRNA expression, mRNA expression and DNA methylation. The regulatory network between miRNAs and mRNAs was constructed followed by the functional analysis of these target mRNAs. Real-time fluorescence quantitative polymerase chain reaction (QRT-PCR) was used to validate the expression of identified miRNAs and mRNAs.
Results: Totally, up to 8 differentially expressed miRNAs, 973 differentially expressed mRNAs and 146 differentially methylated mRNAs were identified. Hsa-mir-222 (degree =33), hsa-mir-221 (degree =29), hsa-mir-214 (degree =13), hsa-mir-138-2 (degree =11) and hsa-mir-34a (degree =4) were miRNAs that regulated the most target mRNAs (such as BCL2, BCL2L11 and PEG3, ALDH1A1, PLA2R1, TFCP2L1, RAB23, TK1 and CTSB). Focal adhesion, MAPK signaling pathway and p53 signaling pathway were three significantly enriched signaling pathways of target differentially expressed mRNAs in the functional analysis. The in vitro validation of hsa-mir-222 and hsa-mir-221, CTSB, TFCP2L1 and BCL2 was consistent with the bioinformatics analysis.
Conclusions: The identified altered miRNAs (hsa-mir-222, hsa-mir-221, hsa-mir-214, hsa-mir-138-2 and hsa-mir-34a) and their target mRNAs (BCL2, BCL2L11 and PEG3, ALDH1A1, PLA2R1, TFCP2L1, RAB23, TK1 and CTSB) may be helpful in understanding the molecule mechanism of follicular variant of papillary thyroid carcinoma.
Methods: The data of miRNA, mRNA and DNA methylation were downloaded from The Cancer Genome Atlas (TCGA) database. Differential analysis between the follicular variant of papillary thyroid carcinoma and controls was performed in terms of miRNA expression, mRNA expression and DNA methylation. The regulatory network between miRNAs and mRNAs was constructed followed by the functional analysis of these target mRNAs. Real-time fluorescence quantitative polymerase chain reaction (QRT-PCR) was used to validate the expression of identified miRNAs and mRNAs.
Results: Totally, up to 8 differentially expressed miRNAs, 973 differentially expressed mRNAs and 146 differentially methylated mRNAs were identified. Hsa-mir-222 (degree =33), hsa-mir-221 (degree =29), hsa-mir-214 (degree =13), hsa-mir-138-2 (degree =11) and hsa-mir-34a (degree =4) were miRNAs that regulated the most target mRNAs (such as BCL2, BCL2L11 and PEG3, ALDH1A1, PLA2R1, TFCP2L1, RAB23, TK1 and CTSB). Focal adhesion, MAPK signaling pathway and p53 signaling pathway were three significantly enriched signaling pathways of target differentially expressed mRNAs in the functional analysis. The in vitro validation of hsa-mir-222 and hsa-mir-221, CTSB, TFCP2L1 and BCL2 was consistent with the bioinformatics analysis.
Conclusions: The identified altered miRNAs (hsa-mir-222, hsa-mir-221, hsa-mir-214, hsa-mir-138-2 and hsa-mir-34a) and their target mRNAs (BCL2, BCL2L11 and PEG3, ALDH1A1, PLA2R1, TFCP2L1, RAB23, TK1 and CTSB) may be helpful in understanding the molecule mechanism of follicular variant of papillary thyroid carcinoma.