Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, Henan, China.
Department of Pathology, Third Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, Henan, China.
Biomed Res Int. 2020 Jan 9;2020:4983420. doi: 10.1155/2020/4983420. eCollection 2020.
Growing evidence shows that dysregulation of miRNAs plays a significant role in papillary thyroid cancer (PTC) tumorigenesis and development. The abnormal expression of miR-384 has been acknowledged in the proliferation or metastasis of some cancers. However, the function and the underlying mechanism of miR-384 in PTC progression remain largely unknown.
Real-time PCR was conducted to detect miR-384 expression in 58 cases of PTC and their adjacent noncancerous tissues. MTT, soft agar assay Transwell assay, and wound-healing assay were carried out to explore the biological function of miR-384 in PTC cell lines of BCPAP and K1. Bioinformatics analysis, dual-luciferase reporter assay, western blot, and functional complementation analysis were conducted to explore the target gene of miR-384. Moreover, Spearman's correlation analysis was conducted to reveal the correlation between miR-384 and PRKACB mRNA in PTC.
The expression of miR-384 decreased obviously in PTC, especially in the tumors with lymph node metastasis or larger tumor size. The ectopic upregulation of miR-384 significantly suppressed PTC progression, and the inhibition of miR-384 had the opposite effects. Moreover, PRKACB gene was confirmed as the target of miR-384.
The study suggests that miR-384 serves as a tumor suppressor in PTC progression by directly targeting the 3'-UTR of PRKACB gene.
越来越多的证据表明，miRNA 的失调在甲状腺乳头状癌（PTC）的发生和发展中起着重要作用。miR-384 的异常表达已被证实与一些癌症的增殖或转移有关。然而，miR-384 在 PTC 进展中的功能和潜在机制在很大程度上仍不清楚。
采用实时 PCR 检测 58 例 PTC 及其相邻非癌组织中 miR-384 的表达。MTT、软琼脂实验、Transwell 实验和划痕愈合实验用于探索 miR-384 在 BCPAP 和 K1 PTC 细胞系中的生物学功能。通过生物信息学分析、双荧光素酶报告基因实验、Western blot 和功能互补分析，探索 miR-384 的靶基因。此外，采用 Spearman 相关分析揭示 miR-384 与 PTC 中 PRKACB mRNA 之间的相关性。
miR-384 在 PTC 中明显下调，特别是在有淋巴结转移或更大肿瘤大小的肿瘤中。miR-384 的异位上调显著抑制了 PTC 的进展，而抑制 miR-384 则产生相反的效果。此外，PRKACB 基因被确认为 miR-384 的靶基因。
该研究表明，miR-384 通过直接靶向 PRKACB 基因的 3'-UTR，在 PTC 进展中发挥肿瘤抑制作用。
