Yang Shujuan, Wang Jing, Ge Wensheng, Jiang Yanfang
Department of Otolaryngology, Liaocheng People's Hospital, Liaocheng, Shandong, China.
Genetic Diagnosis Center, The First Hospital of Jilin University, Changchun, China.
J Cell Biochem. 2018 Aug;119(8):6953-6960. doi: 10.1002/jcb.26902. Epub 2018 May 8.
Laryngeal squamous cell carcinoma (LSCC) is one aggressive malignancy and accounts for 20% of all head and neck cancer. However, the role of LOC554202 in human LSCC remains unknown. The expression level of LOC554202 and miR-31 was detected in the LSCC tiussues by using qRT-PCR. Cell growth was measured by CCK-8 assay. Flow cytometry and matrigel-coated membrane was used to detect for cell cycle and invasion respectively. We indicated that lncRNA LOC554202 expression was overexpressed in LSCC tissues compared with the paired adjacent samples and higher LOC554202 expression was associated with the advanced stage. In addition, we demonstrated that the expression level of miR-31 was downregulated in LSCC tissues compared to the paired adjacent samples and lower miR-31 expression was correlated with the advanced stage. Moreover, the expression of miR-31 was negatively correlated with the expression of LOC554202 in LSCC tissues. Ectopic expression of LOC554202 promoted LSCC cell growth, cell cyle and cell invasion and overexpression of miR-31 inhibited LSCC cell growth, cell cyle and cell invasion. Elevated expression of LOC554202 suppressed miR-31 expression and promoted RhoA expression in LSCC cell, which was a direct target gene of miR-31. Furthermore, LOC554202 increased LSCC cell growth, cell cyle and cell invasion through suppressing miR-31 expression. These results suggested that LOC554202 acted as an oncogene in the development of LSCC.
喉鳞状细胞癌（LSCC）是一种侵袭性恶性肿瘤，占所有头颈癌的20%。然而，LOC554202在人类LSCC中的作用仍不清楚。通过qRT-PCR检测LSCC组织中LOC554202和miR-31的表达水平。采用CCK-8法检测细胞生长情况。分别用流式细胞术和基质胶包被的膜检测细胞周期和侵袭情况。我们发现，与配对的相邻样本相比，lncRNA LOC554202在LSCC组织中表达上调，且较高的LOC554202表达与晚期相关。此外，我们证明，与配对的相邻样本相比，miR-31在LSCC组织中的表达水平下调，且较低的miR-31表达与晚期相关。此外，在LSCC组织中，miR-31的表达与LOC554202的表达呈负相关。异位表达LOC554202可促进LSCC细胞生长、细胞周期进展和细胞侵袭，而过表达miR-31则抑制LSCC细胞生长、细胞周期进展和细胞侵袭。LOC554202表达升高可抑制LSCC细胞中miR-31的表达并促进RhoA表达，RhoA是miR-31的直接靶基因。此外，LOC554202通过抑制miR-31表达增加LSCC细胞生长、细胞周期进展和细胞侵袭。这些结果表明，LOC554202在LSCC发生发展中起癌基因作用。
