C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

Roberta Bulla, Claudio Tripodo, Damiano Rami, Guang Sheng Ling, Chiara Agostinis, Carla Guarnotta, Sonia Zorzet, Paolo Durigutto, Marina Botto () and Francesco Tedesco ()
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Roberta Bulla: University of Trieste
Claudio Tripodo: University of Palermo
Damiano Rami: University of Trieste
Guang Sheng Ling: Centre for Complement and Inflammation Research, Imperial College
Chiara Agostinis: Institute for Maternal and Child Health, Istituto di Ricovero e Cura a Carattere Scientifico Burlo Garofolo
Carla Guarnotta: University of Palermo
Sonia Zorzet: University of Trieste
Paolo Durigutto: University of Trieste
Marina Botto: Centre for Complement and Inflammation Research, Imperial College
Francesco Tedesco: Istituto di Ricovero e Cura a Carattere Scientifico, Istituto Auxologico Italiano

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms10346

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