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. Author manuscript; available in PMC: 2019 Jan 8.
Published in final edited form as: Cancer Res. 2018 Feb 5;78(8):2026–2039. doi: 10.1158/0008-5472.CAN-17-2332

Figure 3. CXCL12γ induces a NE phenotype in PCa and CXCL12γ detection in CTCs of PCa patients.

Figure 3.

A, mRNA levels of N-Myc (MYCN), N-Myc downstream regulated 1 (NDRG1), enolase-2 (ENO2), and synaptophysin (SYP) expression following CXCL12γ overexpressing or control PCa cells as quantified by real-time PCR. B, Protein levels of N-Myc, NDRG1, ENO2, and synaptophysin in CXCL12γ overexpressing or control PCa cells as quantified by Western blots. Examination of NE markers in s.c. tumors generated by CXCL12γ overexpressing or control PCa cells in SCID mice in Fig. 2E. High density of NE cells with extensive vascularization in C, PC3 tumors and D, DU145 tumors were shown by H&E staining. Bar=50μm. ENO2, synaptophysin, and pan-cytokeratin expressing NE cells as detected by IHC staining. Bar=50μm. E, Gene expression of AR-V7, CXCL12γ, and ENO2 in circulating tumor cells (CTCs) isolated from healthy normal control (n=2) and metastatic castration-resistant PCa (mCRPC) patients (n=26) as quantified by real-time PCR. F, Regression analysis between ENO2 and CXCL12γ. Data are representative of mean ± SD (Student’s t-test).