Our study reports a preliminary investigation into the role of human H2
relaxin in prostate
tumor growth. A
luciferase-expressing human
prostate cancer cell line, PC-3, was generated and termed PC3-Luc. PC3-Luc cells were transduced with lentiviral vectors engineering the expression of either
enhanced green fluorescent protein (eGFP) or both H2
relaxin and eGFP in a bicistronic format. These transduced cells were termed PC3-Luc-eGFP and PC3-Luc-H2/eGFP, respectively. To gauge effects, PC3-Luc-H2/eGFP and PC3-Luc-eGFP cells were injected into NOD/SCID mice and monitored over 6 weeks. PC-3
tumor xenografts overexpressing H2
relaxin exhibited greater
tumor volumes compared to control
tumors. Circulating H2
relaxin levels in sera increased with the relative size of the
tumor, with moderately elevated H2
relaxin levels in mice bearing PC3-Luc-H2/eGFP
tumors compared to PC3-Luc-eGFP
tumors. Zymographic analysis demonstrated that
proMMP-9 enzyme activity was significantly downregulated in H2
relaxin-overexpressing
tumors. An advanced angiogenic phenotype was observed in H2
relaxin-overexpressing
tumors indicated by greater intratumoral vascularization by immunohistochemical staining of endothelial cells with anti-mouse CD31. Moreover, PC3-Luc-H2/eGFP
tumors exhibited increased
VEGF transcript by reverse-transcription PCR, compared to basal levels in control animals. Taken together, our study provides the first account of a potential role of H2
relaxin in prostate
tumor development.