Huang Xiaoyong, Shi Haiyan, Shi Xinghai, Jiang Xuemei
Department of Medical Laboratory, Medical College of Yan'an University, Yan'an, 716000, Shaanxi, China.
Department of Laboratory, The First People's Hospital of Urumqi, Ürümqi, 830000, Xinjiang, China.
J Biol Res (Thessalon). 2021 Aug 16;28(1):20. doi: 10.1186/s40709-021-00151-8.
Cervical cancer (CC) is one of the most common and malignant tumors in women. In this study, we aim to explore the role and mechanism of F-box and leucine rich repeat protein 19 antisense RNA 1 (FBXL19-AS1), a novel long-chain non coding RNA (lncRNA) with marked roles in a variety of tumors, in regulating the proliferation and metastasis of CC.
The expression of FBXL19-AS1, miR-193a-5p and COL1A1 were detected by RT-PCR and western blot. Gain- and loss-of functional assays of FBXL19-AS1 and miR-193a-5p were performed in CC cell lines in vitro or in vivo. The proliferation, migration, invasion, apoptosis and epithelial-mesenchymal transition (EMT) of CC cells were determined.
FBXL19-AS1 and COL1A1 were significantly up-regulated in CC tissues, while miR-193a-5p was significantly down-regulated. Overexpression of FBXL19-AS1 significantly promoted the proliferation, migration, invasion, EMT and growth of CC cells and inhibited apoptosis, while knockdown of FBXL19-AS1 had the opposite effects. On the other hand, miR-193a-5p inhibited the proliferation and metastasis of CC cells. Mechanistically, FBXL19-AS1 functioned as a competitive endogenous RNA (ceRNA) and inhibited the expression of miR-193a-5p, which targeted at the 3'-UTR site of COL1A1 and negatively regulated COL1A1 expression.
FBXL19-AS1 promotes the proliferation and metastasis of CC cells by sponging miR-193a-5p and up-regulating COL1A1.
宫颈癌(CC)是女性中最常见的恶性肿瘤之一。在本研究中,我们旨在探讨F-box和富含亮氨酸重复蛋白19反义RNA 1(FBXL19-AS1),一种在多种肿瘤中具有显著作用的新型长链非编码RNA(lncRNA),在调节CC增殖和转移中的作用及机制。
通过RT-PCR和蛋白质印迹法检测FBXL19-AS1、miR-193a-5p和COL1A1的表达。在体外或体内CC细胞系中进行FBXL19-AS1和miR-193a-5p的功能获得和功能缺失实验。测定CC细胞的增殖、迁移、侵袭、凋亡和上皮-间质转化(EMT)。
FBXL19-AS1和COL1A1在CC组织中显著上调,而miR-193a-5p显著下调。FBXL19-AS1的过表达显著促进CC细胞的增殖、迁移、侵袭、EMT和生长并抑制凋亡,而敲低FBXL19-AS1则产生相反的效果。另一方面,miR-193a-5p抑制CC细胞的增殖和转移。机制上,FBXL19-AS1作为竞争性内源RNA(ceRNA)发挥作用并抑制miR-193a-5p的表达,miR-193a-5p靶向COL1A1的3'-UTR位点并负向调节COL1A1的表达。
FBXL19-AS1通过吸附miR-193a-5p并上调COL1A1促进CC细胞的增殖和转移。