YY1 通过长非编码 RNA Kcnq1ot1/miRNA-506-3p/SYPL1 轴加速口腔鳞状细胞癌的进展。
YY1 accelerates oral squamous cell carcinoma progression through long non-coding RNA Kcnq1ot1/microRNA-506-3p/SYPL1 axis.
机构信息
Center for Drug Research and Development, Guangzhou Key Laboratory of Construction and Application of New Drug Screening Model Systems, Key Laboratory of New Drug Discovery and Evaluation of Ordinary Universities of Guangdong Province, Guangdong Pharmaceutical University, No. 280, Waihuan East Road, Guangzhou, 510006, Guangdong, China.
School of Life Sciences and Biophamaceutics, Guangdong Pharmaceutical University, Guangzhou, 510006, Guangdong, China.
出版信息
J Ovarian Res. 2022 Jul 1;15(1):77. doi: 10.1186/s13048-022-01000-5.
OBJECTIVE
Ying Yang1 (YY1) has already been discussed in oral squamous cell carcinoma (OSCC), but the knowledge about its mediation on long non-coding RNA KCNQ1 overlapping transcript 1/microRNA-506-3p/synaptophysin like 1 (Kcnq1ot/miR-506-3p/SYPL1) axis in OSCC is still in its infancy. Hence, this article aims to explain the mechanism of YY1/Kcnq1ot1/miR-506-3p/SYPL1 axis in OSCC development.
METHODS
YY1, Kcnq1ot1, miR-506-3p and SYPL1 expression levels were determined in OSCC tissues. The potential relation among YY1, Kcnq1ot1, miR-506-3p and SYPL1 was explored. Cell progression was observed to figure out the actions of depleted YY1, Kcnq1ot1 and SYPL1 and restored miR-506-3p in OSCC. OSCC tumorigenic ability in mice was examined.
RESULTS
Elevated YY1, Kcnq1ot1 and SYPL1 and reduced miR-506-3p were manifested in OSCC. YY1 promoted Kcnq1ot1 transcription and up-regulated Kcnq1ot1 expression, thereby promoting OSCC cell procession. Silencing Kcnq1ot1 or elevating miR-506-3p delayed OSCC cell progression and silencing Kcnq1ot1 impeded tumorigenic ability of OSCC cells in mice. YY1-mediated Kcnq1ot1 sponged miR-506-3p to target SYPL1.
CONCLUSION
YY1 promotes OSCC cell progression via up-regulating Kcnq1ot1 to sponge miR-506-3p to elevate SYPL1, guiding a novel way to treat OSCC.
目的
Ying Yang1（YY1）已在口腔鳞状细胞癌（OSCC）中进行了讨论，但关于其在长非编码 RNA KCNQ1 重叠转录本 1/微小 RNA-506-3p/突触素样蛋白 1（Kcnq1ot/miR-506-3p/SYPL1）轴介导 OSCC 中的作用仍处于起步阶段。因此，本文旨在解释 YY1/Kcnq1ot1/miR-506-3p/SYPL1 轴在 OSCC 发展中的机制。
方法
测定 OSCC 组织中 YY1、Kcnq1ot1、miR-506-3p 和 SYPL1 的表达水平。探讨 YY1、Kcnq1ot1、miR-506-3p 和 SYPL1 之间的潜在关系。观察耗竭 YY1、Kcnq1ot1 和 SYPL1 以及恢复 miR-506-3p 对 OSCC 细胞进程的作用。检查 OSCC 肿瘤在小鼠中的发生能力。
结果
OSCC 中表现出 YY1、Kcnq1ot1 和 SYPL1 升高和 miR-506-3p 降低。YY1 促进 Kcnq1ot1 转录并上调 Kcnq1ot1 表达，从而促进 OSCC 细胞进程。沉默 Kcnq1ot1 或上调 miR-506-3p 可延缓 OSCC 细胞进程，并抑制 OSCC 细胞在小鼠中的致瘤能力。YY1 介导的 Kcnq1ot1 海绵 miR-506-3p 以靶向 SYPL1。
结论
YY1 通过上调 Kcnq1ot1 来海绵 miR-506-3p 以升高 SYPL1 促进 OSCC 细胞进展，为治疗 OSCC 提供了一种新方法。
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