ERBB2 increases metastatic potentials specifically in androgen-insensitive prostate cancer cells.

摘要: Despite all the blood-based biomarkers used to monitor prostate cancer patients, remains as second common cause of mortality in men United States. This is largely due a lack understanding molecular pathways that are responsible for aggressive forms cancers, castrate-resistant and metastatic cancer. Cell signaling activated by ERBB2 oncogene or RAS frequently found be altered cancers. To evaluate define role ERBB2/RAS pathway metastasis, we have evaluated impact ERBB2- RAS-overexpression on potentials four cell lines derived from tumors with different androgen sensitivities. do so, transfected human DU145, LnCaP, PC3 cells murine Myc-CaP form H-RAS assessed their three complementary assays, wound healing assay, transwell motility invasion assay. We showed while overexpression increased potential androgen-insensitive (i.e. DU145), it did not affect androgen-sensitive LnCaP Myc-CaP). In contrast, only cells, which overexpress c-MYC oncogene. Our data suggest collaborates promote although one critical downstream effectors ERBB2, does phenocopy its lines.