Long noncoding RNA HOTAIR silencing inhibits invasion and proliferation of human colon cancer LoVo cells via regulating IGF2BP2

• Published in: Journal of cellular biochemistry 2019-02, Vol.120 (2), p.1221-1231
• Main Authors: Wu, Xue‐Liang, Lu, Rui‐Yun, Wang, Li‐Kun, Wang, Yuan‐Yuan, Dai, Yong‐Jun, Wang, Chen‐Yu, Yang, Yong‐Jiang, Guo, Fei, Xue, Jun, Yang, Dong‐Dong
• Format: Article
• Language: English
• Subjects: Antisense RNA; Apoptosis; Biomarkers; Cancer; Cell migration; Cell proliferation; Colon; Colon cancer; Colorectal cancer; Density; E-cadherin; epithelial‐mesenchymal transition (EMT); Growth factors; human colon cancer lovo cell; Insulin; insulin‐like growth factor 2 mRNA‐binding protein 2 (IGF2BP2); invasion; long noncoding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR); Mesenchyme; Metastases; proliferation; Proteins; Reporter gene; Ribonucleic acid; RNA; RNA-mediated interference; Transcription; Tumors; Vimentin; Weight
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.27079

Colon cancer is one of the most life‐threatening malignancies worldwide. Long noncoding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) is a cancer‐associated biomarker involved in the metastasis and prognosis of several cancers. However, whether and how HOTAIR affects colon cancer progression is still unclear. Consequently, we used RNA interference to knock down HOTAIR to explore its effects on human colon cancer cells. The dual luciferase reporter gene assay was initially used for testify the regulating relationship between lncRNA HOTAIR and insulin‐like growth factor 2 mRNA‐binding protein 2 (IGF2BP2). We determined the expressions of HOTAIR, IGF2BP2, E‐cadherin, and vimentin. Meanwhile, cell growth, cycle and apoptosis, migration, and invasion were assayed. LoVo cells were transplanted into nude mice, and tumor formation and microvessel density were evaluated. LncRNA HOTAIR positively regulated IGF2BP2. Besides, the expressions of HOTAIR and E‐cadherin and the apoptosis were increased, while the expressions of IGF2BP2 and vimentin, the growth, invasion and migration of LoVo cells, the average tumor weight, and microvessel density value were decreased. Of importance, overexpressed IGF2BP2 could reverse the above impacts. Taken together, the current study indicates that silencing of HOTAIR could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing IGF2BP2 and the epithelial‐mesenchymal transition. Silencing of HOX transcript antisense RNA (HOTAIR) could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing insulin‐like growth factor 2 mRNA‐binding protein 2 (IGF2BP2) and the epithelial‐mesenchymal transition.