Research Paper Volume 13, Issue 10 pp 14065—14077

TCF-3-mediated transcription of lncRNA HNF1A-AS1 targeting oncostatin M expression inhibits epithelial-mesenchymal transition via TGFβ signaling in gastroenteropancreatic neuroendocrine neoplasms

TCF3 down-regulated HNF1A-AS1 and promoted cell migration and invasion. (A) The potential transcription factors of HNF1A-AS1 were predicted by TFbind and RNAreg respectively. The score of each transcription factor was ranked by JASPAR. (B) JASPAR was used to detect the putative binding sites between TCF3 and HNF1A-AS1. (C) qRT-PCR was performed to analyze the level of HNF1A-AS1 in HPNE cell compared with in GEP-NENs cell. (D) Knockdown of TCF3 resulted in decrease of HNF1A-AS1 in GEP-NENs cells. (E) Transwell was performed to investigate the effect of TCF3 knockdown (group e) on GEP-NENs cells migration and invasion. (F–G) Over-expression of HNF1A-AS1 down-regulated cell migration and invasion by transwell and wound healing assay. (H–I) Knockdown of HNF1A-AS1 increased cell migration and invasion by transwell and wound healing assay. *p **p

Figure 5. TCF3 down-regulated HNF1A-AS1 and promoted cell migration and invasion. (A) The potential transcription factors of HNF1A-AS1 were predicted by TFbind and RNAreg respectively. The score of each transcription factor was ranked by JASPAR. (B) JASPAR was used to detect the putative binding sites between TCF3 and HNF1A-AS1. (C) qRT-PCR was performed to analyze the level of HNF1A-AS1 in HPNE cell compared with in GEP-NENs cell. (D) Knockdown of TCF3 resulted in decrease of HNF1A-AS1 in GEP-NENs cells. (E) Transwell was performed to investigate the effect of TCF3 knockdown (group e) on GEP-NENs cells migration and invasion. (FG) Over-expression of HNF1A-AS1 down-regulated cell migration and invasion by transwell and wound healing assay. (HI) Knockdown of HNF1A-AS1 increased cell migration and invasion by transwell and wound healing assay. *p < 0.05, **p < 0.01.