Shen Bin, Ding Haibin, Ye Yanyan, Luo Baozhen
Department of Otolaryngology, Shulan (Hangzhou) Hospital Affiliated to Zhejiang Shuren University, Shulan International Medical College, Hangzhou, Zhejiang, China 310015.
J Oncol. 2022 Apr 21;2022:6406943. doi: 10.1155/2022/6406943. eCollection 2022.
Laryngeal cancer accounts for 25%-30% of tumors in the head and neck. Cystatin SN (CST1) was revealed to show upregulated expression in this cancer, while its functions and upstream pathway remain unknown and need investigation. The current study was designed to solve this problem. We designed short hairpin RNAs targeting CST1 for the loss-of-function assays to probe the influences of CST1 in laryngeal cancer cell proliferation and motility. The upstream competitive endogenous RNA pattern of CST1 was searched using bioinformatics analysis and confirmed by luciferase reporter assays. The experimental results demonstrated that CST1 is a tumor facilitator in laryngeal cancer by stimulating cellular proliferative, migrative, and invasive abilities. CST1 is regulated by the long intergenic non-protein-coding RNA 1278 (LINC01278)/miR-185-5p axis. LINC01278 knockdown and miR-185-5p overexpression exert the same functions as CST1 knockdown to repress cancer cell proliferation, migration, and invasion. In conclusion, LINC01278 plays an oncogenic role in laryngeal cancer by suppressing miR-185-5p to enhance CST1 expression, which enriches the molecular mechanism for the carcinogenesis of laryngeal cancer.
喉癌占头颈部肿瘤的25%-30%。研究发现胱抑素SN（CST1）在这种癌症中表达上调，但其功能和上游通路仍不清楚，需要进行研究。本研究旨在解决这一问题。我们设计了靶向CST1的短发夹RNA用于功能缺失实验，以探究CST1对喉癌细胞增殖和运动的影响。通过生物信息学分析寻找CST1的上游竞争性内源RNA模式，并通过荧光素酶报告基因实验进行验证。实验结果表明，CST1通过刺激细胞的增殖、迁移和侵袭能力，在喉癌中起到肿瘤促进作用。CST1受长链基因间非编码RNA 1278（LINC01278）/miR-185-5p轴调控。LINC01278敲低和miR-185-5p过表达发挥与CST1敲低相同的功能，抑制癌细胞增殖、迁移和侵袭。总之，LINC01278通过抑制miR-185-5p增强CST1表达，在喉癌中发挥致癌作用，这丰富了喉癌发生的分子机制。
