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Article Dans Une Revue Biochimica et Biophysica Acta - Molecular Cell Research Année : 2014

The MUC1 mucin regulates the tumorigenic properties of human esophageal adenocarcinomatous cells

Résumé

MUC1 is a membrane-bound mucin known to participate in tumor proliferation. It has been shown that MUC1 pattern of expression is modified during esophageal carcinogenesis, with a progressive increase from metaplasia to adenocarcinoma. The principal cause of development of esophageal adenocarcinoma is gastro-esophageal re-flux and MUC1 was previously shown to be up-regulated by several bile acids present in reflux. In this report, our aim was thus to determine whether MUC1 plays a role in biological properties of human esophageal cancer cells. For that, a stable MUC1-deficient esophageal cancer cell line was established using a shRNA approach. In vitro (proliferation, migration and invasion) and in vivo (tumor growth following subcutaneous xenografts in SCID mice) biological properties of MUC1-deficient cells were analyzed. Our results show that esophageal cancer cells lacking MUC1 were less proliferative and had decreased migration and invasion properties. These alterations were accompanied by a decreased activity of NFKB p65, Akt and MAPK (p44/42, JNK and p38) pathways. MCM6 and TSG101 tumor-associated markers were also decreased. Subcutaneous xenografts showed a significant decrease in tumor size when cells did not express MUC1. Altogether, the data indicate that MUC1 plays a key role in proliferative, migrating and invasive properties of esophageal cancer cells as well as in tumor growth promotion. MUC1 mucin appears thus as a good therapeutic target to slow down esophageal tumor progression.
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Dates et versions

hal-02905652 , version 1 (29-09-2020)

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Caroline Gronnier, Emilie Bruyère, Fatima Lahdaoui, Nicolas Jonckheere, Michael Perrais, et al.. The MUC1 mucin regulates the tumorigenic properties of human esophageal adenocarcinomatous cells. Biochimica et Biophysica Acta - Molecular Cell Research, 2014, ⟨10.1016/j.bbamcr.2014.06.021⟩. ⟨hal-02905652⟩

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