Zhang Chen-Zheng
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education (KLOBM), School & Hospital of Stomatology, Wuhan University, Luoyu Rd. 237, Wuhan 430079, People's Republic of China.
Biochem Biophys Res Commun. 2017 Aug 5;489(4):404-412. doi: 10.1016/j.bbrc.2017.05.155. Epub 2017 May 28.
Recently, long noncoding RNAs (lncRNAs) have been reported to have crucial regulatory efficiency in human cancer biology. Long intergenic non-coding RNA 668 (LINC00668) was regarded as an oncogene in multiple cancers. However, the underlying molecular mechanism of LINC00668 in oral squamous cell carcinoma (OSCC) has not been studied. In this study, we first demonstrated that LINC00668 expression was up-regulated, which was correlated with tumor progression, and miR-297 down-regulated in OSCC tissues and cells. Importantly, LINC00668 expression was negatively correlated with miR-297 expression in OSCC tissues. Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression. Furthermore, LINC00668 knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67 in vivo. Finally, we confirmed that LINC00668 promoted OSCC activity through VEGFA signaling. In conclusion, these results suggest that LINC00668 promotes OSCC tumorigenesis via miR-297/VEGFA axis, which may provide a new target for the diagnosis and therapy of OSCC disease.
最近，有报道称长链非编码RNA（lncRNAs）在人类癌症生物学中具有关键的调控作用。长链基因间非编码RNA 668（LINC00668）在多种癌症中被视为癌基因。然而，LINC00668在口腔鳞状细胞癌（OSCC）中的潜在分子机制尚未得到研究。在本研究中，我们首先证明LINC00668在OSCC组织和细胞中表达上调，这与肿瘤进展相关，而miR-297表达下调。重要的是，在OSCC组织中LINC00668表达与miR-297表达呈负相关。LINC00668功能缺失表明，LINC00668作为miR-297的竞争性内源RNA（ceRNA）促进VEGFA表达，从而促进OSCC进展。此外，敲低LINC00668可抑制体内肿瘤生长并降低增殖抗原ki-67的表达。最后，我们证实LINC00668通过VEGFA信号通路促进OSCC活性。总之，这些结果表明LINC00668通过miR-297/VEGFA轴促进OSCC肿瘤发生，这可能为OSCC疾病的诊断和治疗提供新的靶点。
