MYB/LINC00092 regulatory axis promotes the progression of papillary thyroid carcinoma.

Lian Cheng, Xian Deng, Yuan Le
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Abstract

Introduction: Thyroid carcinoma is the most frequent malignancy in different endocrine-related tumours. In this study, we demonstrated a long non-coding RNA LINC00092-associated molecular mechanism in promoting the progression of papillary thyroid carcinoma (PTC).

Material and methods: The expression of LINC00092 was analysed in the The Cancer Genome Atlas Thyroid Cancer (TCGA-THCA) patient cohorts and further determined by q-PCR. (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) (MTT) assay, and wound healing assay confirmed the function of LINC00092 in migration and proliferation. Q-ChIP validated the transcriptional target. Luciferase reporter assay validated the miRNA-mRNA target.

Results: The analysis in patient cohorts and in PTC TPC-1 cells showed that the expression of LINC00092 was repressed in thyroid carcinoma. In addition, the expression of LINC00092 was negatively associated with the advanced thyroid TNM stages. LINC00092 repressed epithelial-mesenchymal transition (EMT), migration, and proliferation of TPC-1 cells. Interestingly, we identified that MYB, a well-studied tumour promoter, is a transcription factor of LINC00092, thereby the expression of LINC00092 was directly repressed by MYB. Furthermore, miR-4741 was also validated as a direct target of MYB and was induced by MYB. Notably, LINC00092 was repressed by miR-4741 through the direct 3'-untranslational region (3'-UTR) target. Therefore, MYB induced EMT of TPC-1 cells by repressing LINC00092 directly or indirectly via miR-4741.

Conclusions: Our study validated that LINC00092 is a tumour suppressor lncRNA in PTC. MYB directly or indirectly represses LINC00092, which contributes to the PTC progression. MYB, LINC00092, and miR-4741 form a coherent feed forward loop. The axis of MYB-LINC00092 promotes progression of PTC.

MYB/LINC00092调控轴促进甲状腺乳头状癌的进展。
简介:甲状腺癌是各种内分泌相关肿瘤中最常见的恶性肿瘤:甲状腺癌是各种内分泌相关肿瘤中最常见的恶性肿瘤。在这项研究中,我们证实了与长非编码 RNA LINC00092 相关的促进甲状腺乳头状癌(PTC)进展的分子机制:在癌症基因组图谱甲状腺癌(TCGA-THCA)患者队列中分析了LINC00092的表达,并通过q-PCR进行了进一步测定。(3-[4,5-二甲基噻唑-2-基]-2,5-二苯基四唑溴化物(MTT)试验和伤口愈合试验证实了 LINC00092 在迁移和增殖中的功能。Q-ChIP 验证了转录靶标。荧光素酶报告实验验证了 miRNA-mRNA 靶点:结果:对患者队列和 PTC TPC-1 细胞的分析表明,LINC00092 在甲状腺癌中的表达受到抑制。此外,LINC00092的表达与甲状腺癌TNM分期的晚期呈负相关。LINC00092抑制了TPC-1细胞的上皮-间质转化(EMT)、迁移和增殖。有趣的是,我们发现 MYB(一种已被充分研究的肿瘤启动子)是 LINC00092 的转录因子,因此 LINC00092 的表达直接受到 MYB 的抑制。此外,miR-4741 也被证实是 MYB 的直接靶标,并被 MYB 诱导。值得注意的是,miR-4741 通过直接的 3'- 非翻译区(3'-UTR)靶点抑制了 LINC00092。因此,MYB通过直接或间接抑制LINC00092,从而诱导TPC-1细胞的EMT:我们的研究验证了 LINC00092 是 PTC 中的肿瘤抑制 lncRNA。结论:我们的研究验证了 LINC00092 是 PTC 中的肿瘤抑制 lncRNA。MYB、LINC00092和miR-4741形成了一个连贯的前馈环。MYB-LINC00092 轴促进了 PTC 的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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