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, Francesco Tedesco

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Article number10346
JournalNature Communications
Volume7
DOIs
Publication statusPublished - Feb 1 2016

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)
  • Physics and Astronomy(all)

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