Skip to main content
. 2012 Jun 7;33(10):1897–1908. doi: 10.1093/carcin/bgs198

Fig. 2.

Fig. 2.

PTEN regulates CSF-1 expression via PI 3 kinase/Akt signaling. (A and D) MDA-MB-231 breast cancer cells were transfected with vector alone or HA-tagged PTEN plasmids. The conditioned media from vector- and PTEN-transfected cells were used for ELISA to detect CSF-1 protein (panel A). Mean ± SE of triplicate measurements is shown. *P = 0.036 versus control. Total RNAs from these cells were examined for CSF-1 mRNA by qRT–PCR as described in the Materials and methods (panel D). Mean ± SE of triplicate measurements is shown. *P = 0.007 versus control. (B, C, E and F) MDA-MB-231 breast cancer cells were transfected with vector or dominant negative PI 3 kinase (HA-tagged ∆p85: panels B and E) or dominant negative Akt (HA-tagged K179M; panels C and F). The conditioned media were used for ELISA to detect CSF-1 protein (panels B and C) (29). Mean ± SE of triplicate measurements is shown. *P = 0.0042 and 0.0128 versus control, respectively. Total RNAs from these cells were examined for CSF-1 mRNA by qRT–PCR as described in Materials and methods (panels E and F). Mean ± SE of triplicate measurements is shown. *P = 0.0019 and 0.0263 versus control respectively. Bottom panels show expression of PTEN, ∆p85 and Akt K179M. PI 3 kinase/Akt signal transduction regulates CSF-1 transcription (panels G to I). MDA-MB-231 mammary cancer cells were transfected with CSF-1-Luc reporter and either PTEN (panel G) or ∆p85 (panel H) or Akt K179M (panel I). The cell lysates were assayed for luciferase activity as described in Materials and methods (23,24,29,30). Mean ± SE of triplicate measurements is shown. *P = 0.0012 versus control in panel G; *P = 0.0268 versus control in panel H; *P = 0.0203 versus control in panel I. Bottom panels show expression of HA-tagged PTEN, ∆p85 and Akt K179M in representative samples.