Int J Biol Sci 2012; 8(3):383-393. doi:10.7150/ijbs.3579
Interleukin-11 Promotes the Progress of Gastric Carcinoma via Abnormally Expressed Versican
1. Department of Biochemistry and Molecular Biology, Second Military Medical University, Shanghai 200433, China;
2. Department of Pharmacology, Zhejiang Chinese Medical University, Hangzhou 310053, China;
3. Department of Medical Oncology, Changzheng Hospital, Shanghai, 200070, China.
# These authors contributed equally to this paper.
Versican, a ubiquitous component of the extracellular matrix (ECM), accumulates both in tumor stroma and cancer cells and is highly regulated by various cytokines. The aberrant expression of versican and its isoforms is known to modulate cell proliferation, differentiation, and migration, all of which are features of the invasion and metastasis of cancer; versican is also known to favour the homeostasis of the ECM. Interleukin-11 (IL-11) is an important cytokine that exhibits a wide variety of biological effects in gastric cancer development. Here, we analysed the expression of versican isoforms and found that the major isoforms expressed by both gastric carcinoma tissue and gastric cell lines were V0 and V1, and V1 was significantly higher in gastric carcinoma tissue. The treatment of the gastric cell lines AGS and MKN45 with rhIL-11 resulted in a significant increase in the expression of V0 and V1. Exogenous IL-11 increased migration in AGS and MKN45 cells, whereas these effects were reversed when the expression of V0 and V1 were abolished by siRNA targeting versican V0/V1. Collectively, these findings suggest that the abnormally expressed versican and its isoforms participate, at least in part, in the progress of gastric carcinoma triggered by IL-11.
Keywords: Versican, IL-11, gastric carcinoma, migration.
Zhang Z, Zhang J, Miao L, Liu K, Yang S, Pan C, Jiao B. Interleukin-11 Promotes the Progress of Gastric Carcinoma via Abnormally Expressed Versican. Int J Biol Sci 2012; 8(3):383-393. doi:10.7150/ijbs.3579. Available from http://www.ijbs.com/v08p0383.htm