N-Myc Promotes Angiogenesis and Therapeutic Resistance of Prostate Cancer by TEM8

Abstract Although patients with early localized prostate cancer can achieve a longer survival, castration-resistant prostate cancer (CRPC) has gradually developed with the use of androgen deprivation therapy (ADT). N-Myc and TEM8 play an important role in the progression of several cancer types. However, the underlying mechanism of how N-Myc and TEM8 promote the progression of prostate cancer remains unclear. In this study, the expression of N-Myc and TEM8 were detected in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) tissues by immunohistochemistry (IHC). To find the mechanism of prostate cancer resistance to treatment, LNCaP cell lines were maintained in RPMI 1640 medium supplemented with 10% Charcoal-stripped fetal Bovine Serum. Subsequently, R language software was used to verify our results. Tubule formation assay of human umbilical vein endothelial cell (HUVEC) was conducted to examine the effect of N-Myc and TEM8 overexpression on angiogenesis of prostate cancer cells.IHC results showed a positive correlation between the expression of N-Myc and TEM8 in prostate cancer tissues. Further analysis showed that N-Myc and TEM8 were associated with clinicopathological features and poor prognosis in prostate cancer patients. We found that the overexpression of N-Myc and TEM8 promotes proliferative ability and angiogenesis. Further, N-Myc and TEM8 overexpression was associated with therapeutic resistance. N-Myc promoted angiogenesis and therapeutic resistance in prostate cancer via TEM8. Hence, targeting N-Myc/TEM8 pathway in prostate cancer would be a novel therapeutic strategy to advance the treatment of prostate cancer patients.