Department of Dermatology, Institute of Dermatology and Venereology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.
Department of Dermatology, Affiliated Hospital of Southwest Medical University, Luzhou, China.
J Cell Biochem. 2018 Dec;119(12):10393-10405. doi: 10.1002/jcb.27388. Epub 2018 Aug 26.
Cutaneous squamous cell carcinoma (CSCC), an epidermal keratinocyte-derived skin tumor, is one of the most leading causes of cancer-associated morbidity and mortality worldwide. Long noncoding RNAs have emerged as key regulators of tumor development and progression. Recent studies have identified LINC00319, a long intergenic noncoding RNA, as an oncogene in lung cancer. However, the biological role of LINC00319 in CSCC remains largely unknown. The current study aimed to explore the role of LINC00319 in CSCC and uncover the molecular mechanisms. In current study, we found that LINC00319 was significantly upregulated in both CSCC tissues and cell lines. Besides, the χ test showed that increased expression of LINC00319 was associated with larger tumor size, advanced TNM stage, and lymphovascular invasion. Gain-of-function and loss-of-function approaches were applied to investigate the effects of LINC00319 on CSCC cells. Functional studies demonstrated that LINC00319 promoted CSCC cell proliferation, accelerated cell cycle progression, facilitated cell migration and invasion, and inhibited cell apoptosis. Mechanistic studies revealed that LINC00319 exerts its oncogenic functions in CSCC via miR-1207-5p-mediated regulation of cyclin-dependent kinase 3. Taken together, upregulation of LINC00319 implies a potential link with poor prognosis and reflects CSCC progression. Collectively, this study may provide some evidence for LINC00319 as a candidate target in CSCC treatment.
皮肤鳞状细胞癌 (CSCC) 是一种表皮角质形成细胞来源的皮肤肿瘤，是全球癌症相关发病率和死亡率的主要原因之一。长非编码 RNA 已成为肿瘤发生和发展的关键调节剂。最近的研究表明，长非编码 RNA LINC00319 是肺癌中的一种癌基因。然而，LINC00319 在 CSCC 中的生物学作用在很大程度上仍然未知。本研究旨在探讨 LINC00319 在 CSCC 中的作用，并揭示其分子机制。在本研究中，我们发现 LINC00319 在 CSCC 组织和细胞系中均显著上调。此外，卡方检验表明，LINC00319 的表达增加与肿瘤体积增大、TNM 分期较晚和淋巴管血管侵犯有关。采用功能获得和功能丧失方法研究 LINC00319 对 CSCC 细胞的影响。功能研究表明，LINC00319 促进 CSCC 细胞增殖，加速细胞周期进程，促进细胞迁移和侵袭，并抑制细胞凋亡。机制研究表明，LINC00319 通过 miR-1207-5p 介导的细胞周期蛋白依赖性激酶 3 调节发挥其致癌作用。总之，LINC00319 的上调与不良预后有潜在联系，并反映了 CSCC 的进展。综上所述，本研究可能为 LINC00319 作为 CSCC 治疗的候选靶点提供了一些证据。
