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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Long noncoding RNA AFAP1-AS1 acts as a competing endogenous RNA of miR-423-5p to facilitate nasopharyngeal carcinoma metastasis through regulating the Rho/Rac pathway

Fig. 8

FOSL2 modulates the transcription of LASP1 through binding its promoter. a. Prediction of potential FOSL2 binding sites in the LASP1 promoter. The nucleotides that are consensus FOSL2 binding sequences (WT) and mutated sequences (MT) are indicated. b. The luciferase activity of the LASP1 promoter and the AP-1 transcription factor was measured in 5-8F and HNE2 cells cotransfected with the FOSL2 overexpression vector or siFOSL2 and luciferase reporters containing the AP-1 luciferase plasmid (pAP1), or the WT or MT LASP1 promoter, as indicated. Overexpression of FOSL2 significantly induced the LASP1 and AP-1 transcription activity. *p < 0.05, **p < 0.01, compared with normal control (NC) group. c. The AP-1 transcription activity was examined through transfection of the AFAP1-AS1 overexpression vector or siAFAP1-AS1 and the AP-1 reporter plasmid containing the AP-1 consensus sequence. AP-1 transcriptional activity was induced through overexpressing AFAP1-AS1 or reduced after knockdown of AFAP1-AS1. d. The expression of LASP1 and AFAP1-AS1 was regulated by FOSL2 after knockdown or overexpression of FOSL2

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