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. Author manuscript; available in PMC: 2011 May 3.
Published in final edited form as: Cancer Res. 2010 Jan 12;70(2):471–480. doi: 10.1158/0008-5472.CAN-09-2863

Figure 3. The role of CXCL12 and PGK1 on NSF and PCa proliferation and invasion.

Figure 3

Figure 3

Figure 3

(A) Expression of CXCL12 or PGK1 in NSFs induces proliferation. NSFs and CAFs with altered levels of CXCL12 and PGK1 were evaluated for the expression of Ki-67 as an indicator of proliferation. Representative Ki-67 staining (brown, nuclear) is presented with Hematoxylin used as a counterstain. Original magnification 20×, where the black bars represents 100 μM.

(B) Expression of CXCL12 or PGK1 in NSFs induces PCa cell proliferation. After a 24 h serum starvation, PCa cells (PC3) were washed and 1×105 cells were plated. CM derived from CAF β-gal, CAFsiPGK1, CAFsiCXCL12, NSFCXCL12, or NSFPGK1 and NSFControl cells were overlaid onto the PCa cells . Proliferation was evaluated by XTT staining over a five day period. *Denotes significant difference from NSF and CAF controls (p<0.05, ANOVA) for mean ± SE of n=5 samples per condition.

(C) PCa invasion regulated by CXCL12 or PGK1 expressed by NSFs. PC3 cells were placed in the top chamber of invasion plates containing a reconstituted extracellular matrix in serum-free RPMI medium, and CM derived from NSFCXCL12, NSFPGK1 and NSFControl or CAFCXCL12, CAFPGK1 and CAFControl or CAFsiCXCL12, CAFsiPGK1 and CAFβ-gal cells were added to the lower chambers. Invasion was determined at 48 h by MTT staining and the data are presented as % invasion ± standard deviation for n=5. *Denotes significant difference from invasion between alterations of CXCL12 or PGK1 expression vs. controls (p<0.05, ANOVA).