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. Author manuscript; available in PMC: 2010 Nov 13.
Published in final edited form as: Cell. 2009 Oct 29;139(4):693–706. doi: 10.1016/j.cell.2009.10.014

Figure 3.

Figure 3

Let-7a is down-regulated during transformation by NF-κB.

(A) RNA levels of individual let-7 family members in cells treated with TAM for the indicated times.

(B) Levels of let-7a RNA in untreated and TAM-treated (36h) cells in the presence or absence of NF-κB inhibitor (5 μM BAY-117082 and 6 μM JSH-23).

(C) Lin28B protein levels (western blot) in ER-Src cells at the indicated times after TAM treatment.

(D) Lin28B mRNA levels (mean ± SD) during transformation in the presence or absence of an NF-κB inhibitor (5 μM BAY-117082).

(E) Levels of precursor RNAs (pri-let-7a and pri-let-7d/f) in untreated and TAM-treated cells.

(F) NF-κB occupancy (fold-enrichment) at the Lin-28B and let-7a loci as determined by chromatin immunoprecipitation of crosslinked cells that were or were not treated with TAM.

(G) Luciferase activity (mean ± SD)) of Lin28B vector containing the NF-κB binding site during transformation.

(H) Luciferase activity of Lin28B vector (wt, mutated or deleted in NF-κB site) in TAM-treated (36h) cells.

(I) Anchorage-independent growth assays (microscopic counting of 50 μm colonies) of untreated and TAM-treated cells transfected with the indicated let-7 family members or siRNA against Lin28B.