Akt1 governs breast cancer progression in vivo

Opposing roles of the oncogene Akt isoforms in tumour progression: is there a dark side to Akt pathway inhibition?

“…Consistent with the above study, other in vivo studies using Akt1 knockout mice resulted in fewer metastases, with the conclusion that Akt1 signalling is positively associated with invasion leading to metastasis [16]. A study of constitutively active Akt1 in the mouse mammary gland by Hutchinson et al reported that Akt1 suppresses mammary tumor invasion [14].…”

Nuclear Factor-κB Enhances ErbB2-Induced Mammary Tumorigenesis and Neoangiogenesis in Vivo

“…DNA synthesis was analyzed by [ 3 H] thymidine (TdR) incorporation as previously described. 31,32 S phase was analyzed by flow cytometry. The Annexin V-PE apoptosis detection kit (BD Biosciences, Franklin, NJ) was used according to the manufacturer's protocol, followed by flow cytometry.…”

“…31 Images were captured using an Olympus (Tokyo, Japan) BX61 confocal microscope. Vessels were quantified at ϫ200 using a linear encoded motorized Dr. John Ojelfo (Georgetown University, Washington, DC) provided the XY stage (Prior, NJ).…”

Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells

“…Several genes that are required for the development and maintenance of epithelial polarity have been identified including hDlg1 that plays an important role in controlling cell polarization during oriented migration of epithelial cells [19]. Most of the biological functions of hDlg1 rely on its interaction with several regulatory proteins, including ezrin–radixin–moesin (ERM) complex, which participates in cytoskeletal remodeling during cellular migration [20,21]. The normal distribution of hDlg and phosphorylated ERM can be disrupted by ErbB2 overexpression [21].…”

“…Most of the biological functions of hDlg1 rely on its interaction with several regulatory proteins, including ezrin–radixin–moesin (ERM) complex, which participates in cytoskeletal remodeling during cellular migration [20,21]. The normal distribution of hDlg and phosphorylated ERM can be disrupted by ErbB2 overexpression [21]. …”