Skip to main content
. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Nat Rev Gastroenterol Hepatol. 2013 Jul 16;10(10):607–620. doi: 10.1038/nrgastro.2013.120

Figure 4.

Figure 4

Tumour cells crosstalk with stromal cells via mucins. Neoplastic developments elicit a proinflammatory and hypoxic environment leading to a desmoplastic and fibrotic reaction and enhanced mucin expression (1).41,76,118–122 Aberrantly upregulated mucins sterically hide the tumour-associated antigens from invading macrophages, neutrophils and cytotoxic T cells (2), and indirectly protect tumour cells from the cytotoxic effects of activated immune effector cells (3). TAG72 and CA125 modulate M2 macrophages to an immunosuppressive phenotype (4). Aberrantly localized mucins interact and impart stability to various RTKs and aggravate oncogenic signalling (5). MUC1 cytoplasmic tail, through interactions with a variety of proteins, mediates oncogenic signalling (6); its interaction with galectins promotes tumour cell survival during metastasis by avoiding killing by NK cells and helps in extravasation through interaction with ICAM1 (7). Similarly, MUC4 and MUC16 interactions facilitate metastasis (7). Overexpression of mucins and the hypoxic environment in pancreatic tumour cells leads to the production of various factors, that in turn, remodel the extracellular matrix and induce neoangiogenesis (8). Abbreviations: MMP, matrix metalloproteinase; PanIN, pancreatic intraepithelial neoplasias; RTK, receptor tyrosine–protein kinase.