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Abstract
Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mice. Bone marrow (BM) chimeras between C1qa−/− and WT mice identify non-BM-derived cells as the main local source of C1q that can promote cancer cell adhesion, migration and proliferation. Together these findings support a role for locally synthesized C1q in promoting tumour growth.
Highlights
Complement C1q is the activator of the classical pathway
The involvement of C in cancer immunosurveillance has long been neglected until monoclonal antibodies to tumour-associated antigens were introduced in cancer therapy[21]
We have recently reported that C1q favours trophoblast invasion of maternal decidua[39] and promotes angiogenesis in wound healing[40]
Summary
Complement C1q is the activator of the classical pathway. it is recognized that C1q can exert functions unrelated to complement activation. We searched for metastatic melanoma cells in the lungs, the organ preferentially colonized by the cancer cells that escape from the primary tumour site, and detected metastases in 6 out of 11 WT mice but only in 1 out of 11 C1qa À / À mice (Fig. 5e–f).
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