Skip to main content
. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Cancer Res. 2021 Sep 30;81(23):6018–6028. doi: 10.1158/0008-5472.CAN-21-0030

Figure 4. MiR-205 was involved in ENT-induced SALL4 inhibition.

Figure 4.

(A) miRNA sequencing results of H661 cells after 8 hours treatment with 2.5 μM ENT or DMSO. (B) miR-205 was up-regulated by ENT and predicted to target SALL4 by the Targetscan database. (C) Real-time PCR of miR-205 expression in H661 cells after 2.5 μM ENT or DMSO treatment for 8 hours. U6 was used as a normalization control. (D) ChIP-qPCR of the miR-205 promoter region and non-specific control region after 2.5 μM ENT treatment. IgG was used as a normalization control. (E) Sequence of wild-type SALL4 3’UTR with miR-205 binding site or mutant one without binding site. (F) Luciferase reporter result in 293T cells after transfection with the indicated vectors. (G) mRNA and (H) protein levels of SALL4 in H661 cells after transfection with miR-205 or non-specific control. (I) Cell viability of H661 cells after indicated treatment for 5 days. (J) Flow cytometry of H661 cells after the indicated treatment. (K) Percent apoptotic and dead cells in (J). (L) Cell viability of ENT pre-treated H661 cells after transfection of miR-205 or non-specific control. (M) Flow cytometry of ENT pre-treated H661 cells after indicated treatment. (N) Percent apoptotic and dead cells in (M). n.s. means P>0.05, *P<0.05, **P<0.01, ***P<0.001, N=3.