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ER-resident oxidoreductases are glycosylated and trafficked to the cell surface to promote matrix degradation by tumour cells.

Abstract：

:Tumour growth and invasiveness require extracellular matrix (ECM) degradation and are stimulated by the GALA pathway, which induces protein O-glycosylation in the endoplasmic reticulum (ER). ECM degradation requires metalloproteases, but whether other enzymes are required is unclear. Here, we show that GALA induces the glycosylation of the ER-resident calnexin (Cnx) in breast and liver cancer. Glycosylated Cnx and its partner ERp57 are trafficked to invadosomes, which are sites of ECM degradation. We find that disulfide bridges are abundant in connective and liver ECM. Cell surface Cnx-ERp57 complexes reduce these extracellular disulfide bonds and are essential for ECM degradation. In vivo, liver cancer cells but not hepatocytes display cell surface Cnx. Liver tumour growth and lung metastasis of breast and liver cancer cells are inhibited by anti-Cnx antibodies. These findings uncover a moonlighting function of Cnx-ERp57 at the cell surface that is essential for ECM breakdown and tumour development.

journal_name

Nat Cell Biol

journal_title

Nature cell biology

authors

Ros M,Nguyen AT,Chia J,Le Tran S,Le Guezennec X,McDowall R,Vakhrushev S,Clausen H,Humphries MJ,Saltel F,Bard FA

doi

10.1038/s41556-020-00590-w

subject

Has Abstract

pub_date

2020-11-01 00:00:00

pages

1371-1381

issue

11

eissn

1465-7392

issn

1476-4679

pii

10.1038/s41556-020-00590-w

journal_volume

22

pub_type

杂志文章

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