Functional Genomics Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
Cancer Lett. 2013 May 1;331(2):230-8. doi: 10.1016/j.canlet.2013.01.003. Epub 2013 Jan 20.
Here in, we investigated the mechanism underlying overexpression of miR-135b in the human head and neck squamous cell carcinoma (HNSCC) cell lines and in the HNSCC mouse model. Exogenous expression of miR-135b in these cell lines increased cell proliferation, migration, and colony formation. Gene silencing analysis revealed that miR-135b affects a regulator that inhibits hypoxia-inducible factor (HIF). Increased miR-135b expression was positively correlated with HIF-1α expression and microvessel density in the HNSCC model. Thus, our data demonstrate that miR-135b acts as a tumor promoter by promoting cancer cell proliferation, colony formation, survival, and angiogenesis through activation of HIF-1α in HNSCC.
在这里，我们研究了 miR-135b 在人头颈鳞状细胞癌 (HNSCC) 细胞系和 HNSCC 小鼠模型中过度表达的机制。外源性表达 miR-135b 可增加这些细胞系的细胞增殖、迁移和集落形成。基因沉默分析表明，miR-135b 影响一种抑制缺氧诱导因子 (HIF) 的调节剂。miR-135b 表达增加与 HNSCC 模型中 HIF-1α 表达和微血管密度呈正相关。因此，我们的数据表明，miR-135b 通过激活 HIF-1α 促进 HNSCC 中的癌细胞增殖、集落形成、存活和血管生成，从而发挥肿瘤促进作用。
