Fig. 3: RXRα drives the transcription of KRT7-AS and the RXRα agonist berberine promotes KRT7-AS expression. | Cell Death & Disease

Fig. 3: RXRα drives the transcription of KRT7-AS and the RXRα agonist berberine promotes KRT7-AS expression.

From: The long non-coding RNA keratin-7 antisense acts as a new tumor suppressor to inhibit tumorigenesis and enhance apoptosis in lung and breast cancers

Fig. 3

The KRT7-AS genomic DNA fragment (−1600 to +400) from the transcription initial site was separated into seven fragments (A, left panel). Luciferase assay showed that the fragments which contain the transcription factor RXRα-binding site had promoter activity (A, right panel), and indicated that the promoter DNA from −1600 to −1350 from the transcription initial site was the shortest fragment with strong promoter activity (A, B). LASAGNA method indicated that the DNA fragment from -1600 to -1350 has six putative transcription factor binding sites (B), The core nucleic acids GGTCA in wild type of RXRα-binding site in the sub-fragment P6 (C) was mutated to AAAAC (D). Luciferase assay showed that both deletion and mutation the core nucleic acids CGAGGGTCAGCCC in the RXRα-binding site lost the promoter activity (E, F). RXRα levels were detected in RXRα-silenced A549 cells (G). KRT7-AS levels were detected in RXRα-silenced A549 cells (H). The RXRα agonist berberine significantly increased KRT7-AS transcription levels (I), and concurrently raised PTEN protein levels (J, K). Data are shown as mean ± SD of three independent replicates. *P < 0.05, **P < 0.01, ***P < 0.001.

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