An Immunoregulatory Role for Complement Receptors in Murine Models of Breast Cancer.

The complement system has demonstrated roles in regulating tumor growth, although these may differ between tumor types. The current study used two murine breast cancer models (EMT6 and 4T1) to investigate whether pharmacological targeting of receptors for complement proteins C3a (C3aR) and C5a (C5aR1) is protective in murine breast cancer models. In contrast to prior studies in other tumor models, treatment with the selective C5aR1 antagonist PMX53 had no effect on tumor growth.

TWEAK/Fn14 promotes apoptosis of human endometrial cancer cells via caspase pathway.

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible immediate-early response protein 14 (Fn14) have been detected in several human tumors, and demonstrated to regulate multiple cellular responses, including proliferation, survival, migration, apoptosis and differentiation, suggesting roles in cancer. The objective of this study was to clarify the role of TWEAK/Fn14 in the development of human endometrial cancer. We found that TWEAK gene expression was down-regulated and Fn14 gene expression was up-regulated in human endometrial cancer specimens compared with that in normal endometrial specimens; TWEAK acting on Fn14 decreased cell viability by inducing apoptosis through caspase pathways in endometrial cancer cells.