Skip to main content
. Author manuscript; available in PMC: 2020 Dec 1.
Published in final edited form as: Gastroenterology. 2019 Aug 20;157(6):1646–1659.e11. doi: 10.1053/j.gastro.2019.08.018

Figure 5. KDM3A transcriptionally regulates mRNA expression of DCLK1, a pancreatic stem cell marker.

Figure 5.

(A) A boxplot showing KDM3A is upregulated in PDAC comprised of normal pancreatic tissue (n=46) and primary pancreatic adenocarcinomas (n=145) (p < 0.01). The data is acquired through microarray analysis performed by Moffitt et al.

(B) A boxplot showing significantly increased expression of DCLK1 in TCGA PDAC (PAAD) samples as compared to the normal pancreas (TCGA-PAAD normal and GTEx pancreas) (p < 0.05).

(C) The TCGA database showed a positive correlation between KDM3A and DCLK1 in PDAC (R = 0.29, p < 0.01).

(D) Knockdown of KDM3A in S2–007 cells (shRNA2 and shRNA3) showing the reduced expressions of KDM3A and DCLK1.

(E) Clustergram of RNA-seq data of HPNE overexpressed HPNE and S2–007 cells showing DCLK1 upregulation in PDAC cells associated with KDM3A overexpression.

(F) ChIP assay using KDM3A antibody shows one site at the promoter and another in Exon 1 in DCLK1 that is pulled down by anti-KDM3A antibody. The HIF-responsive element (HRE) is located in the promoter region downstream from the RG3 site.