Homophilic interaction of cd147 promotes il-6-mediated cholangiocarcinoma invasion via the nf-κb-dependent pathway

10Citations
Citations of this article
9Readers
Mendeley users who have this article in their library.

Abstract

Cholangiocarcinoma (CCA), an aggressive cancer of bile ducts, is a well-known chronic inflammation-related disease. The major impediment in CCA treatment is limited treatment options for advanced disease; hence, an alternative is urgently required. The role of CD147 on cytokine production has been observed in inflammation-related diseases, but not in CCA. Therefore, this study was focused on CD147-promoting proinflammatory cytokine production and functions. Proinflammatory cytokine profiles were compared between CD147 expressing CCA cells and CD147 knockout cells (CD147 KO). Three cytokines, namely interleukin (IL)-6, IL-8, and granulocyte–monocyte colony-stimulating factor (GM-CSF), were dramatically diminished in CD147 KO clones. The involvement of the CD147-related cytokines in CCA invasion was established. CD147-promoted IL-6, IL-8, and GM-CSF secretions were regulated by NF-κB nuclear translocation, Akt activation, and p38 phosphorylation. CD147-fostering IL-6 production was dependent on soluble CD147, CD147 homophilic interaction, and NF-κB function. The overexpression of specific genes in CCA tissues compared to normal counterparts emphasized the clinical importance of these molecules. Altogether, CD147-potentiated proinflammatory cytokine production leading to CCA cell invasion is shown for the first time in the current study. This suggests that modulation of CD147-related inflammation might be a promising choice for advanced CCA treatment.

Cite

CITATION STYLE

APA

Dana, P., Kariya, R., Lert-Itthiporn, W., Seubwai, W., Saisomboon, S., Wongkham, C., … Vaeteewoottacharn, K. (2021). Homophilic interaction of cd147 promotes il-6-mediated cholangiocarcinoma invasion via the nf-κb-dependent pathway. International Journal of Molecular Sciences, 22(24). https://doi.org/10.3390/ijms222413496

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free