PRL and DNA damage alter the immune response to breast cancer cells

摘要: There are conflicting reports of the role prolactin in breast cancer, and its within context tumour microenvironment is not well understood. In our previous study, we demonstrated a cross-talk between ataxia telangiectasia-mutated (ATM) DNA damage response pathway PRL-Janus-kinase-2 (JAK2)-signal transducer activator transcription-5 (STAT5)-heat shock protein-90 (HSP90) pathway. order to investigate PRL initiation effect vivo, used model cancer that assesses ability cells initiate orthotopic xenograft formation after damage. Breast engineered secrete human or control cells, were treated with damaging agent doxorubicin vehicle injected into mammary fat pad immune deficient SCID mice. secretion from did change latency compared controls, although combined treatment increased latency. Injection natural killer (NK) cell-depleting antibody, anti-asialo GM1, resulted faster only PRL-secreting pre-treated doxorubicin, PRL-only empty vector controls. These results may shed light on demonstrate at least cell damage, exposure does delay initiation, but together reduced volume over time due asialo-GM1-positive cells.