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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Cancer Prev Res (Phila). 2009 Dec 22;3(2):190–201. doi: 10.1158/1940-6207.CAPR-09-0229

Figure 5. DNA Damage Induces Activin A, COX-2 and Growth Arrest in p16-Competent HMEC.

Figure 5

A) HMEC were exposed to 100μM Etoposide (RM40, RM45, RM46) or to 60J/m2 of UVC (RM45) as described in Figure 1A. Line graphs indicate relative COX-2 and activin A mRNA levels and activin A protein levels in conditioned media compared to the untreated control. B) Activin A, COX-2, p16 and p21 mRNA levels in parent, vector (pWP1) or TRF2-HMEC (CM7, RM146). C) Population doublings in HMEC (CM7) infected with lentivirus containing TRF2 or empty vector (pWP1) or parent HMEC. D) Overview of the DNA damage-dependent COX-2 induction and its consequences in HMEC (intact p16/Rb) or vHMEC (silenced p16).