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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Cancer Res. 2011 Nov 11;72(1):165–175. doi: 10.1158/0008-5472.CAN-11-2552

Figure 4. Regulation of p18INK4c by E2F1.

Figure 4

A. Relative levels of INK4c, INK4a and CDC6 RNAs in Hs68 cells infected with a retrovirus encoding SV40 large T-Ag (LT) or empty vector control (Vec) (left panel). Lysates from the same cells were fractionated by SDS-PAGE and immunoblotted for p18INK4c and p16INK4a as indicated (right). B. Survey of p18INK4c and p16INK4a expression in a series of human cancer cell lines from different anatomical sites: breast (T47D, BT5499, ZR75-1 MDA-MB468 and MCF7), keratinocyte (HaCaT), bladder (K5637 and T24), cervix (C33A), bone (U2OS) and prostate (DU145 and PC3). The +/− below each lane refers to the functional status of the RB1 gene in these cell lines, based on published literature. CDK4 was used as a loading control. C. Comparison of E2F1 RNA (left) and protein (right) levels in proliferating (P) and senescent (S) HDFs (TIG3). D. Comparison of INK4c and E2F1 RNA expression in HDFs (IMR90) infected with a retrovirus encoding H-RASG12V (Ras) or empty vector (Vec). E. Down-regulation of E2F1 protein in HDFs (TIG3) cells transduced with H-RASG12V. F. Down-regulation of E2F1 in HDFs infected with a retrovirus encoding HA-p16INK4a.

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