CDK9 promotes transcription of HOTAIR in cancers
(A) HOTAIR expression was significantly inhibited after inhibiting CDK9 by LDC-067 in PDAC, HCC, and CRC cells. (B and C) ChIP analysis revealed that the occupancies of (B) H3K4me3 and (C) RNA PolII Ser2 phosphorylation on Ex-CGI were greatly decreased after inhibiting CDK9. (D) The nuclear accessibility to the 3′ end of HOTAIR gene was inhibited after inhibition of CDK9 in PDAC, HCC, and CRC cells. MspI mimicked the binding of RNA PolII to the HOTAIR gene. (E) Nuclear run-on qPCR analysis revealed the transcription elongation efficiency of HOTAIR after inhibition of CDK9 in PDAC and HCC cells. The expression of exon 6 was compared with the expression of exon 2. Transcription efficiency of exon 6 was decreased after inhibition of CDK9. Data are from at least three independent experiments and plotted as means ± SD. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.