Skip to main content
. Author manuscript; available in PMC: 2013 Mar 15.
Published in final edited form as: Int J Cancer. 2011 Aug 26;130(6):1459–1469. doi: 10.1002/ijc.26152

Figure 2. LLL12 inhibited STAT3 DNA binding activity and expression of downstream targets associated with proliferation and survival of MM tumor cells.

Figure 2

(A) U266 and ARH-77 MM cells were treated in LLL12 (2.5μM) or DMSO for 24 hours and nuclear extracts were examined for DNA binding activity. LLL12 induced statistically significant (*) reductions in STAT3 DNA binding activity, results are representative of two independent experiments in each cell line. (B) U266 and ARH-77 human MM cell lines were cultured in LLL12 (5 μM) or DMSO for 24 hours. Reverse transcriptase PCR revealed decreased expression of STAT3 target genes in LLL12-treated cells as compared to DMSO control following treatment with LLL12. (C) Downstream STAT3 target proteins, Cyclin D1, Survivin, Bcl-2, and DNMT1 were downregulated by LLL12 as shown by western blot analysis. (D) MM.1S cells were stimulated with IL-6 (2.5–10 ng/ml) for 48 hours in the presence or absence of LLL12 (2.5μM) for the last 24 hours. Reverse transcriptase PCR showed IL-6 enhanced expression of STAT3 target genes, which was blocked by LLL12.